What Should I Believe?

evidenceIf you’ve been following along with my blogs over the past couple of years, you’ve probably noticed one thing. None of the conclusions I find are particularly exciting, alarming, or new.

Typically, extraordinary claims turn out to be false. If it sounds too good (or too bad) to be true, it probably is. With the exception of minor nuance, the status quo and the general medical consensus are usually right on point.

Why? Because we really do have expert scientists testing medical and nutritional ideas constantly. Contrary to what some fringe doctors would have you believe, the mainstream medical community does not have the wool pulled over their eyes. They are not being duped by pharmaceutical companies. There is nothing that “your doctor doesn’t want you to know”.

Every now and then, mainstream scientific consensus is proven wrong. However, this is the exception and not the rule. When proven wrong, the scientific consensus changes. Science doesn’t have an agenda. People, however, do not readily change their minds when the science changes.

I could get deep into the psychology of why people believe things that are not likely to be true. But, let’s just accept the fact that we have all been susceptible to false beliefs at some time. Everyone needs to be careful to make sure they aren’t persuaded by anecdotes or quasi-scientific research and jargon (or worse; fooled by charlatans, “fake news”, or conspiracies).

To illustrate my point, here’s a peer reviewed article demonstrating how unlikely conspiracy theories are to be true.

On the Viability of Conspiratorial Beliefs (2016) https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0147905

Of course, not all false information out there can be classified as a “conspiracy theory”. Much of what we find in the nutrition realm are simply unproven hypotheses being pushed by people who stand to make a few bucks, or even doctors who have anecdotal evidence that their methods work. Their logic may seem sound, but at the end of the day, their advice is not proven to work better than the status quo.

Many professionals use cherry-picked studies and misinterpreted science to convince people that their treatments are legitimate.


That’s why you have to use the scientific method in order to find out what’s true. You have to ask the question (Does X work best?) first and then look for all the research. If you start with the answer (X works best) and then look for supporting evidence, your conclusion may be inaccurate. You may find the 5% of research that supports X and miss the 95% of research that doesn’t.

However, when people get really excited about an idea or when they are trying to sell a product, they go about the research in the wrong order. They only look for materials to support their claims. That puts the responsibility on the consumer to do the research the right way. The best way to do this is the way I research topics for my blog. However, I understand that peer-reviewed databases aren’t for the faint of heart.

Here is a list of some of my favorite lay-person-friendly fact-checking websites for high quality medical and nutritional information:

Sciencebasedmedicine.org: This is one of the best sites on the internet. It’s a wonderful source of truth for all things medial. The authors crack down on fraud and hype, and pseudoscience in logical and easy-to-understand articles.

Quackwatch.org: This site keeps a list of quack physicians and links to help you understand why they can’t be trusted.

Snopes.com: This is a reliable source of information for all claims that need fact-checking.

Rationalwiki.org: This is another good source for fact-checking on topics ranging from nutrition to politics to conspiracy theories.

Nutrition Diva (quick and dirty tips podcast or website): She’s covered every nutrition topic under the sun in her weekly podcasts which are usually about 8 minutes long. Her insights are research based, balanced, and practical.

Google: If you start hearing about some new nutrition claim that sounds too good (or too bad) to be true, just google it with the words “fact check” or “quack”. Take a look at what the opposition has to say before blindly believing Karen in accounting.

I’ll end with a quote from Steven Novella of Science-Based Medicine.

“Complementary and alternative medicine is complementary and alternative medicine because it is not science-based. If it were, it would not be “alternative” medicine; it would be medicine.”


Considering Keto?

ketogenic-dietThe claim

Ketogenic diets are the best way to lose weight and improve health

The ketogenic diet has been around for decades, but was popularized by Dr. Atkins in the late 1990s. Recently, it has become all the rage again.

Initial Google Search

What is the ketogenic diet?

It’s a low carb, moderate protein, high fat diet that helps your body use fat for fuel instead of sugar. People practicing a ketogenic diet usually eat about 75% fat, 20% protein, and only 5% carbs. Meanwhile, a typical American diet consists of around 35% fat, 15% protein, and 50% carbs.

Five percent is equal to 20-50 grams of carbs per day depending on your size. In food terms, one banana can contain more than your quota of carbs for an entire day.

What foods do people eat on a ketogenic diet?

You can eat any type of meat, fish, eggs, cheese, butter, non-starchy vegetables, leafy greens, avocados, nuts, seeds, and some berries. You can’t eat any sort of grains, legumes, sugars, most fruits, or starchy vegetables.

What happens inside your body when you drastically reduce carbohydrates?

Your body learns to rely on fat for energy. This is referred to as “ketosis”. When there are no carbs in your bloodstream, your insulin drops. The drop in insulin allows fat cells to be released into the blood stream. Then your body breaks down fat cells in the liver and turns them into ketones for your cells to run on instead of glucose.

If you read my last blog on fasting, you know that experts don’t completely agree on when the body is burning fat, sugar, or even muscle. But, the intermittent fasting and ketosis camp swears that the body doesn’t start burning fat until you’re in ketosis which can mean up to a week of almost no carbs.

How do you know when you’re in ketosis?

Some people use a blood glucose monitor (more accurate) or urine test strips (less accurate). Other signs include increased urination, dry mouth, bad/sweet breath, reduced hunger, and increased energy (after about a week).

Here is what proponents say:

  1. Ketogenic diets help you lose body fat by making your body use fat instead of sugar for fuel and by keeping you from feeling hungry.
  2. You will improve your heart health by increasing HDL (good cholesterol) and decreasing LDL (bad cholesterol), triglycerides, and blood pressure. It may also increase the size of your LDL, which makes the particles less dangerous.
  3. Your brain will function better. Not only will you be able to think more clearly and feel more alert, but you may also decrease your risk for developing Parkinson’s and Alzheimer’s disease.
  4. You will reduce your risk for developing cancer. The ketogenic diet will cause oxidative stress in cancer cells and it will reduce cancers associated with blood sugar or insulin problems.
  5. You’ll have clearer skin. Some forms of acne are thought to be related to blood sugar.
  6. It reduces seizures in children with epilepsy.
  7. It improves fertility in women with polycystic ovarian syndrome (PCOS)
  8. It can help people with type 2 diabetes manage their blood sugar and insulin levels, and maybe even stop needing medication.
  9. Your energy levels will improve.

However, many doctors and experts state the following in regards to keto:

  1. You lose muscle
  2. You become extremely fatigued
  3. You will enter “starvation mode” and stop losing weight
  4. You mostly lose water weight on keto
  5. It may slightly hinder athletic performance
  6. It’s hard to stick to because it eliminates so many foods
  7. It can cause damage to the heart
  8. If you have underlying kidney or liver problems, keto will make them worse
  9. You’ll be more likely to die prematurely from heart disease, stroke or cancer

Follow-up Questions

  1. Calories being equal, do people lose more fat on keto or non-keto diets?
  2. How do results hold up long term?
  3. Which claims are true? Which ones are hype or biased?
  4. I’ve read people who eat the fewest carbs are more likely to die prematurely. Are there confounding factors? Maybe people on keto were already more overweight or more at-risk.

Peer Reviewed Research

Inclusion criteria: Human clinical trials or meta-analyses of studies that compare a ketogenic diet to a traditional low calorie diet with the purpose of improving markers of metabolic syndrome. I did not include studies on healthy-weight people, athletes, or people with cancer, dementia, PCOS, or other special populations. The ketogenic diet is generally accepted by the medical community as effective for controlling epilepsy and slowing the growth of some types of cancer.

  1. Very-low-carbohydrate ketogenic diet v. low-fat diet for long-term weight loss: a meta-analysis of randomised controlled trials. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23651522

This is a review of 13 randomized controlled trials, which compared a ketogenic group to a low-fat calorie restricted group. After a 1 year follow up, the people in the ketogenic group achieved greater weight loss and lower blood pressure than the low-fat group.

2. Long term successful weight loss with a combination biphasic ketogenic Mediterranean diet and Mediterranean diet maintenance protocol. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24352095

This study included 89 overweight subjects. They cycled between a 20-day ketogenic diet and longer maintenance periods of the Mediterranean diet for a year. The subjects lost and kept off 22 pounds on average. All markers of metabolic syndrome improved and all but 8 subjects were able to comply with the diet.

3. Metabolic impact of a ketogenic diet compared to a hypocaloric diet in obese children and adolescents. (2012) https://www.ncbi.nlm.nih.gov/pubmed/23155696

This study compared 58 overweight children and adolescents. Half were assigned to a ketogenic group and half to a traditional calorie restricted group. The study lasted 6 months. In the end, all participants improved health markers and lost weight. The ketogenic group had better improvements than the calorie restricted group.

4. Comparison of a very low-calorie-ketogenic diet with a standard low-calorie diet in the treatment of obesity. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24584583

This study compared a ketogenic diet group with a reduced-calorie diet group. After 2 months, the ketogenic group lost an average of 29 pounds while the reduced calorie diet lost about 11 pounds. After a year, the group that had participated in the ketogenic group had lost an average of 44 pounds and the reduced calorie group only lost about 15. The ketogenic group preserved lean muscle mass and did not have any lasting side effects. This data was not reported for the other group.

5. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes. (2012) https://www.ncbi.nlm.nih.gov/pubmed/22673594

This study included 363 overweight people. 102 of them had type 2 diabetes. Subjects were allowed to choose whether they wanted to be in the keto group or the low-calorie group. Results were measured after 24 weeks. Both diets improved markers of metabolic syndrome, but the keto group had more significant results. Many diabetics were able to decrease or discontinue their medication.

6. Short-term safety, tolerability and efficacy of a very low-calorie-ketogenic diet interventional weight loss program versus hypocaloric diet in patients with type 2 diabetes mellitus. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27643725

This study divided 89 overweight men and women into a keto group and a low-calorie group. After 4 months, results were measured. They found that the ketogenic diet was more effective in reducing body weight and improving glucose than the low calorie diet. It was also tolerated well by participants with diabetes.

7. A randomized trial of a low-carbohydrate diet vs orlistat plus a low-fat diet for weight loss. (2010) https://www.ncbi.nlm.nih.gov/pubmed/20101008

This study included 146 overweight men who were divided into a keto group and a low-calorie plus orlistat (weight loss pill) diet. Subjects followed the diets for 48 weeks. Both groups had similar improvements in weight loss and blood glucose. The ketogenic diet was more effective for lowering blood pressure.

What We Know and Don’t Know

The research I found shows that the ketogenic diet is safe and effective for weight loss. In every study I found, it was more effective than a normal low-calorie diet. People on a ketogenic diet were able to improve all aspects of metabolic syndrome. No adverse health effects were reported in any human studies. These studies were robust, well-controlled, and measured effects after a reasonable amount of time (4-12 months).

In my analysis, I only included research comparing the ketogenic diet to another more traditional diet in overweight humans. However, I did read some studies on mice, athletes, cancer patients, etc. In general, the diet was safe and effective for all groups. Athletes tended to have improved cardiovascular performance without losing strength or muscle mass. Research on cancer and neurodegenerative disorders was in the preliminary phase. Many ideas and hypotheses were presented, but I found few clinical trials. However, the diet seems promising for at least some people with these conditions. Studies also found that keto improved symptoms of PCOS in some patients.

The research also confirmed that participants feel less hungry on the ketogenic diet than on traditional diets and that most participants were able to adhere to the diet.

Research in mice, however, did present some concerns. First, the diet seemed to cause problems with normal fertility, pregnancy, and lactation. Second, it caused biotin deficiency which can cause rashes, hair loss, depression, and other problems. However, this can be avoided by taking B vitamin supplements. Third, the ketogenic diet seemed to cause non-alcoholic fatty liver disease. These problems were not confirmed in human trials and may or may not be applicable.

Conclusions and Applications

Research supporting the ketogenic diet for weight loss is overwhelmingly positive. I would say that even though I personally felt like crap when I tried to go keto (I don’t think I ever got my carbs quite low enough), it’s definitely worth a try for most people with weight loss goals. I particularly like the idea of cycling keto with a low-calorie Mediterranean diet. For me, that sounds sustainable and may be a good way to avoid the potential for vitamin deficiency. It will be interesting to learn more about how doctors implement keto for treatment of conditions like cancer and Alzheimer’s in the future.

Should I Try Intermittent Fasting?

What is Intermittent Fasting (IF)?

This is a popular term for several different diet plans. Each one is made up of windows of feeding and windows of fasting. For example, one of the most popular IF schedules is to eat between 12pm and 8pm and fast for the remaining 16 hours of the day. Some people choose to eat during a smaller or larger window or during different times of the day. Another popular way to implement intermittent fasting is to have two days per week where you fast or eat very few calories while eating normally the remaining 5 days.

You could also choose to try a longer fast. Some people fast for a week, a month, or more. The longest fast on record is from 1973. A 27-year-old man fasted for 382 days. He lived on nothing but water, tea, coffee, and nutritional supplements and went from 456 to 180 pounds (AND he only regained about 15 pounds after 5 years). However, professionals monitored his health closely and made sure he stayed healthy. Keep in mind that many people have died, often from heart failure, after fasting for as little as a month.

The Claim

Intermittent fasting is a good idea because it will help you burn body fat without constantly feeling hungry, keep metabolism high, and repair/prevent disease.

Initial Google Search

In order to understand why some experts think IF is the best diet plan, you need to know how the body stores energy. When you eat, your insulin increases and remains high for 3-5 hours during digestion. During this time, some of the food energy is used up by cells right away, some of it is stored as glycogen in the liver or muscles, and some of it is stored as body fat. The liver and muscles can’t store very much glycogen (only around 2,000 calories), but the body can store unlimited amounts of fat.

When you stop eating, your body turns primarily to the stored glycogen in your liver to keep itself going. Typically, after 3-5 hours, your insulin drops and you get hungry and eat again. The process starts over. Some experts believe that by eating every 3-5 hours, your body never gets a chance to use any of its body fat. You only burn easy-to-access glucose (made from the glycogen stored in the liver).

During my online research, I’ve seen many different ideas on when the body burns glycogen versus when it burns fat stores. Some experts believe no body fat is actually burned until you’ve been fasting for at least 48 hours and are in ketosis (My blog on the ketogenic diet is next in queue. Hold your horses). Other sources say the body starts burning fat just after you’ve finished digesting the previous meal and insulin levels have dropped (around 4 hours after eating). Some sources say the body is always burning both glucose and fat, but the ratio varies based on when you’ve last eaten and your activity level. Still other sources say that you burn fat while you’re sleeping even if your glycogen stores are full. Seriously, how is there no consensus on this?

Sources also vary as to whether or not your body will turn to muscle for fuel after it’s used the glycogen in the liver. Some are convinced this happens immediately after glycogen is depleted while others say this is very rare.

The idea behind fasting is that your body will finally get the chance to rely on stored body fat for fuel rather than glycogen from the liver or muscles.

Of course, the most commonly accepted weight loss method is calorie restriction. When you eat fewer calories, you lose weight. However, as we all know, it’s not quite that simple. Proponents of intermittent fasting are quick to point out that when someone starts dieting, they first lose glycogen stores, which contain several pounds of water. They say that actual fat loss won’t begin until glycogen is depleted.

Additionally, they cite a well-accepted phenomenon known as “adaptive thermogenesis”. This, put simply, is when the body learns to function with fewer calories per day. It’s also known as “decreased metabolism” or more recently, “The Biggest Loser Effect” (Former Biggest Loser contestants say they have to keep their caloric intake restricted to under 1000 calories a day in order to maintain their weights). This adaptive effect is thought to be irreversible. The effect is somewhat proportional to how extremely a person has dieted, but experts disagree on how much a person’s metabolic rate can really drop. Many experts acknowledge a 10-15% drop in metabolic rate, while others put that number closer to 40-50%.

One of the purported benefits of intermittent fasting is that it helps you burn fat while keeping the metabolism high. Some doctors say you will lose fat even if you continue to eat the same number of calories as before. Others say that you still need to decrease your overall calorie intake to lose fat, but, even when you stop fasting, your metabolism will still be as high as other same-weight people.

Here are the main claims made by IF supporters (most of these benefits are said to be attainable by fasting 12-24 hours at a time, depending on the source):

  1. Fat loss: Insulin levels remain low, making stores of body fat accessible which leads to fat loss
  2. Increased metabolism: Your metabolic rate will remain constant or even increase
  3. Autophagy: The body will get rid of old/damaged cells or cell parts when there is limited energy to keep them running. This is supposed to improve the body’s ability to heal itself from long-term injury and may even help prevent cancer and Alzheimer’s Disease by getting rid of damaged cells and protein buildup.
  4. Growth hormone: human growth hormone increases by up to 5 times. This prevents muscle breakdown and helps build new, healthy cells.
  5. Increases lifespan: It is well documented that calorie restriction increases lifespan. This may be true for IF as well. This is thought to work by changing “gene expression” which means fewer signs of aging and age-related diseases.
  6. Decreased hunger hormone: Ghrelin, the hunger hormone, tends to show up at times we are accustomed to eating. If you get your body used to eating in a smaller window, you will stop feeling hungry during other times. If you fast for more than a couple days, ghrelin will disappear.

Follow-up Questions:

  1. How true are the claims above?
  2. Can you lose fat while eating on a normal schedule (every 3-5 hours for 16 hours out of the day)? If so, how likely are you to end up with a slower metabolism?
  3. Does your body really need to deplete all of its glycogen before it can start burning body fat? If so, how is it possible that people on low-fat diets (think vegans) are able to lose fat?
  4. Does autophagy ever occur when you are not fasting?
  5. I’ve heard most of the research supporting IF has been done on mice. Do human studies show the same results?

Peer Reviewed Research (Click here to skip to analysis)

1.Effects of intermittent fasting on body composition and clinical health markers in humans. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26374764

This review analyzed several different studies that looked at different types of intermittent fasting. They found that alternate day fasting resulted in improvements in body weight, body fat, total cholesterol, triglycerides, and blood lipids. However, results were modest. People lost only 3-9% of their body weight after 3 to 24 weeks. This is does not seem to be any better than any other kind of diet. Additionally, researchers stated that results on time-restricted feeding were limited and inconclusive. No comments were made about metabolism changes or autophagy.

2. Health effects of intermittent fasting: hormesis or harm? A systematic review. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26135345

This review found three randomized controlled trials and two observational studies that met criteria. All 5 studies found modest improvements in body weight and other metabolic risk factors. The authors concluded that the current literature supports intermittent fasting, but that much more research in humans is needed before the use of fasting as a health intervention can be recommended. Again, this study did not address the questions of metabolism changes or autophagy.

3. Intermittent fasting vs daily calorie restriction for type 2 diabetes prevention: a review of human findings. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24993615

This review wanted to compare IF to traditional calorie restricted diets to determine which approach would be better for decreasing type 2 diabetes risk factors. The researchers found similar improvements between the two types of diets in visceral fat mass, fasting insulin, and insulin resistance. They found that traditional calorie restricted diets were better for decreasing body weight than IF.

4. INTERMITTENT FASTING AND HUMAN METABOLIC HEALTH (2015) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4516560/

This review analyzed 13 other studies which used different types of intermittent fasting. Their goal was to make suggestions for where to go next with the research. Some of the conclusions they drew from analyzing the studies were:

All fasting protocols resulted in modest clinically significant weight loss and none seemed to do any physical or mental harm.

There is significant rodent data supporting time-restricted feeding, but these studies have not been replicated in humans

IF has not been shown to be superior to calorie restricted diets in any way

There are little or no published data linking IF with reduced incidences of diabetes, heart disease, cancer, Alzheimer’s disease or other chronic diseases.

5. Practicality of intermittent fasting in humans and its effect on oxidative stress and genes related to aging and metabolism. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25546413

This study looked at whether IF (alternate day fasting) would act on the same pathways as calorie restriction in order to extend life span and ameliorate age-related diseases. The study was 6 weeks long and anti-oxidant supplements were used for 3 of the 6 weeks. Their results showed mild increases in certain gene expressions associated with longevity, but most of these did not reach clinical significance.

6. Repetitive stimulation of autophagy-lysosome machinery by intermittent fasting preconditions the myocardium to ischemia-reperfusion injury. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26103523

This is a mouse study which shows that IF induces autophagy in the heart.

7. Roles of caloric restriction, ketogenic diet and intermittent fasting during initiation, progression and metastasis of cancer in animal models: a systematic review and meta-analysis. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25502434

This is a review of 59 different mouse studies. Calorie restriction and ketogenic diet were found to “play an anti-cancer role” in 90% of the relevant studies. Only 60% of the studies looking at IF found a similar anti-cancer role. Researchers concluded that calorie restriction and ketogenic diets are better at fighting cancer than intermittent fasting.

8. Chronic intermittent fasting improves cognitive functions and brain structures in mice. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23755298

This is a mouse study that found that IF mice had better learning and memory than control mice.

9. Fasting: molecular mechanisms and clinical applications. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24440038

This is a summary of bacteria, rodent, and human studies. It states that IF results in: reduced oxidative damage and inflammation, optimized energy metabolism, and protection from diabetes, cancer, heart disease and neurodegeneration. It states that in humans, IF has been shown to reduce obesity, hypertension, asthma, and rheumatoid arthritis.

10. Effects of intermittent fasting on metabolism in men. (1992) https://www.ncbi.nlm.nih.gov/pubmed/23582559

This article reviewed older literature on IF. It states that animal models showed positive changes in glucose and lipid metabolism. In humans, it has shown a decrease in inflammation, lower oxidative stress, and better adherence than traditional diets.

11. Do intermittent diets provide physiological benefits over continuous diets for weight loss? A systematic review of clinical trials. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26384657

This review looked at studies that compared calorie restriction diets to IF diets. Their main goal was to see whether IF diets were better at keeping metabolism high like they claim. They concluded that IF diets “do not appear to attenuate adaptive responses to energy restriction or improve weight loss efficiency” and that they work, but are not superior to calorie-restricted diets.

12. Caloric restriction and intermittent fasting alter hepatic lipid droplet proteome and diacylglycerol species and prevent diabetes in NZO mice. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25645620

This is a mouse study that used mice that were predisposed to developing diabetes. One group of mice was fed a 10% calorie restricted diet, one was fed with alternate day IF, and one group was fed a regular control diet. None of the mice on calorie restriction of IF developed diabetes while 43% of the control group did.

13. Intermittent fasting combined with calorie restriction is effective for weight loss and cardio-protection in obese women. (2012) https://www.ncbi.nlm.nih.gov/pubmed/23171320

This study found that IF plus calorie restriction is an effective weight loss strategy and that it words slightly better with a liquid diet.

14. Effects of Intermittent Fasting, Caloric Restriction, and Ramadan Intermittent Fasting on Cognitive Performance at Rest and During Exercise in Adults. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26438184

This study provided data showing that fasting during daylight hours may impair cognitive function and memory. This was not found with calorie-restricted diets.

15. Intermittent fasting during Ramadan attenuates proinflammatory cytokines and immune cells in healthy subjects. (2012) https://www.ncbi.nlm.nih.gov/pubmed/23244540

This study found that Ramadan-style fasting reduced overall inflammation. Researchers did not compare results to a control group or a calorie-restricted group.

16. Food restriction by intermittent fasting induces diabetes and obesity and aggravates spontaneous atherosclerosis development in hypercholesterolaemic mice. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24176004

This study compared mice that were prone to heart disease with wild-type mice. Each type of mouse was fed with alternate day fasting, which resulted in an overall 20% decrease in calories. Each group also had control mice, which were fed a normal diet. In the wild mice, IF reduced markers of heart disease. However, in the mice that were heart-disease prone, markers of heart disease increased by as much as 3 times. Researchers concluded that alternate day fasting is not beneficial for mice with hypercholesterolemia.

17. Intermittent fasting: a “new” historical strategy for controlling seizures? (2013) https://www.ncbi.nlm.nih.gov/pubmed/23206889

This study is based on the idea that ketogenic diets can help children with epilepsy. Researchers thought IF may help in a similar way. In 4 out of 6 children studied, “transient improvements” were seen in seizure control with some “hunger-related adverse reactions”.

18. Fasting therapy for treating and preventing disease – current state of evidence. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24434759

This review goes over the benefits of fasting that have been observed in research. The author states IF can help improve: rheumatic diseases, chronic pain syndromes, hypertension, metabolic syndrome, and possibly cancer. He states that deceleration or prevention of most chronic degenerative and chronic inflammatory diseases can be achieved through IF or traditional calorie restriction. He goes over possible mechanisms for these health benefits including promotion of autophagy and decreased oxidative stress.

19. Intermittent fasting dietary restriction regimen negatively influences reproduction in young rats: a study of hypothalamo-hypophysial-gonadal axis. (2013)https://www.ncbi.nlm.nih.gov/pubmed/23382817

This study discussed how IF caused infertility in rats and how this could apply to humans.

20. Impact of intermittent fasting on glucose homeostasis. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27137896

This review looked at 4 case studies of fasting and found no improvements in blood glucose.

21. Could Intermittent Energy Restriction and Intermittent Fasting Reduce Rates of Cancer in Obese, Overweight, and Normal-Weight Subjects? A Summary of Evidence. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27422504

This review confirms that calorie restriction helps reduce cancer rates in animal and human studies. Researchers tried to determine whether IF would reduce cancer rates even further. Some mice studies show that it does. They confirmed that some studies show that IF leads to greater improvements in insulin sensitivity than calorie restriction. However, the authors thought the evidence was not strong enough to recommend the use of IF over calorie restriction.

22. Intermittent fasting does not affect whole-body glucose, lipid, or protein metabolism. (2009) https://www.ncbi.nlm.nih.gov/pubmed/19776143

This study compared a small number of people who were on an IF diet with a small group on a “standard diet”. After 2 weeks, no differences were noted between the 2 groups in terms of body weight, blood glucose, or insulin sensitivity. They did note a decrease in metabolism during rest in the IF group which they concluded might lead to weight gain.

23. Metabolic Effects of Intermittent Fasting. (2017) https://www.ncbi.nlm.nih.gov/pubmed/28715993

This article summarized the health benefits of IF supported by literature. They state that IF promotes weight loss and may improve metabolic health. They concluded that IF may be beneficial to improving health in the general population. They did not compare IF with traditional calorie restriction.

24. Comparison of High-Protein, Intermittent Fasting Low-Calorie Diet and Heart Healthy Diet for Vascular Health of the Obese. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27621707

This study tested 40 obese adults. They were all put on a high-protein, low calorie IF diet for 12 weeks. Then half of them stayed on a maintenance IF diet while the other half was put on a maintenance “heart healthy” diet for a year. The IF group had less weight regain and better “arterial compliance” at the end of the year than the group on the heart healthy diet.

25. Fasting and refeeding differentially regulate NLRP3 inflammasome activation in human subjects. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26529255

This study found that IF is useful for reducing inflammation in obese patients. They acknowledged that calorie-restricted diets do the same.

26. The effect of fasting on indicators of muscle damage. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23266375

This study tested 29 participants after strength training. Half ate a controlled diet before measurements were taken while half fasted for 8 hours. No major differences were noted in signs/symptoms of muscle damage, but researchers said fasting may “generally affect common indirect markers of muscle damage”.

27. Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. (2005) https://www.ncbi.nlm.nih.gov/pubmed/15741046

This article reviews the benefits of IF and calorie restriction: extended lifespan, increased resistance to age-related diseases, improved health in overweight people, reduced risk factors for stroke and heart disease, and increased insulin sensitivity. They review some of the mechanisms of how this works and state that they may be similar to the way exercise works to improve health. These mechanisms are: reduced oxidative damage and increased cellular stress resistance. It does not prefer one diet method over the other.

28. Intermittent fasting and caloric restriction ameliorate age-related behavioral deficits in the triple-transgenic mouse model of Alzheimer’s disease. (2007) https://www.ncbi.nlm.nih.gov/pubmed/17306982

This is a mouse study that found that both calorie restriction and IF diets can protect against age-related deficits in cognitive function.

What We Know and Don’t Know

Taken together, the majority of the evidence shows that any form of calorie restriction will improve health and longevity. Intermittent fasting does not appear to be superior to traditional calorie restriction, but it is a safe and healthy option for most people. It turns out fat loss and insulin sensitivity can be increased with or without fasting, as long as calories are reduced. Additionally, the research does not support the notion that your metabolism will be protected by choosing IF over calorie restriction. Both diets seem to slow metabolism. Both diets also seem to upregulate autophagy, even without fasting. Many of the research studies with the most exciting conclusions associated with IF were done on mice. Their findings overall do apply to humans, but to a lesser extent. This is common with rodent research since humans are more complex and more difficult to control.

I was unable to answer several of my research questions. I still don’t know when the body switches from burning glucose to burning fat or whether both are being burned all the time at different rates. The research shows that people do burn fat without having to fast for 12-48 hours to completely deplete their glycogen stores. Otherwise, how would people who are not fasting ever be able to lose fat? I didn’t find much information regarding an upregulation of human growth hormone on either diet. I also wasn’t able to find much on ghrelin, the hunger hormone. Studies varied on whether people were able to tolerate traditional diets or IF more easily in regards to feeling hungry.

Conclusions and Applications

The main take-away here is that a reduced calorie diet has a lot of health benefits. These include: resistance to heart disease, diabetes, obesity, cancer, Alzheimer’s disease, and other effects of aging. Intermittent fasting does not seem to have any unique benefits. However, it may help some people reduce calories. It’s important to keep in mind that these results were not only seen in overweight people and animals. Even people of healthy weights were protected by reduced calorie diets that were below what was needed to maintain their weight. This evidence suggests that all healthy weight and overweight people would benefit from reducing calorie intake even though their metabolisms will likely slow due to adaptation.

How Safe is Fluoride?

Another hot topic in the natural health community is fluoride. As you probably know, some countries, including the U.S., Australia, and Canada, add a small amount of fluoride to the public water supply. In the U.S., this practice began in 1945 after scientists noticed that people living in areas with more natural fluoride in the ground water had fewer cavities. In 1962, the practice of adding fluoride to city water supplies became widespread. Some European countries followed suit by fluoridating their water, milk or salt supplies.

Today, this practice is highly controversial among the public. Much of the scientific community cites research showing that fluoride decreases tooth decay. Skeptics claim that fluoride causes a myriad of health problems ranging from weak bones to cancer to impaired brain development. We’ll look more into all of these claims in more depth later.

What is fluoride exactly? Fluorides are compounds that combine the element fluorine with another substance, usually a metal. The types of fluoride added to different water systems include fluorosilicic acid, sodium fluorosilicate, and sodium fluoride.

Fluoride is often found naturally in water, soil, and even air. The amount of fluoride found in ground water can range from 0 to more than 13 parts per million (ppm) (which is the same as saying 13 milligrams per liter (mg/L)). Higher amounts are usually found in rural areas of developing nations including India and China.

Here in the U.S., as in most other developed nations who purposefully add fluoride to their drinking water, the level is around 0.7ppm.

How does fluoride work? It is widely accepted that applying fluoride topically and then spitting it out can help reduce tooth decay by helping the tooth enamel re-mineralize and by impairing bacteria’s ability to eat away at the enamel. The mechanism by which ingested fluoride works is somewhat controversial, but dentists say it works in 2 ways. The first way is by adding fluoride to the inside of children’s teeth while they are forming. The second way is by keeping a very low amount of fluoride in the saliva at all times which can act on the tooth enamel topically.

The Claim

Adding fluoride to the public water system can cause a variety of serious health problems.

Initial Google Search

Organizations claiming fluoridation is harmful:

First, let’s take a look at what the opposition has to say. Some prominent agencies and personalities that claim fluoride is a threat to public health include:  Global Healing Center, Fluoride Action Network, The Center for Natural Dentistry, Dr. Mercola, and Dr. Axe.

First, they say fluoride weakens skeletal health. They claim that the liver cannot process fluoride so it remains in the bloodstream, leeches calcium from bones and causes a condition called skeletal fluorosis. Babies and children excrete less fluoride from their kidneys and absorb up to 80% of ingested fluoride into their bones. Children in fluoridated communities have twice as many bone defects as children who are not. Fluoride also increases hip fractures in the elderly.

Second, they say it causes osteoarthritis by calcifying bone cartilage.

Next, they claim fluoride is toxic to thyroid and pineal gland. The thyroid can absorb fluoride which inhibits its function. Lowered thyroid function has been found in otherwise healthy people at 2.3 ppm. Fluoride was used in the 1800s to reduce thyroid function in people with overactive thyroid. The pineal gland regulates body rhythms and sleep-wake cycles. Fluoride accumulates here and calcifies the gland reducing its function over time.

They claim harm to reproductive health. Fluoride accelerates female puberty due to damage in the pineal gland. Higher levels of fluoridated water consumption correlate to lower fertility rates. Fluoride at high doses damages sperm. Men living in highly fluoridated areas have lower levels of testosterone.

Another claim is reduced kidney health. Higher rates of chronic kidney disease have been reported in areas where water contains high levels of fluoride.

They state that Fluoride causes inflammation and atherosclerosis (heart disease)

They cite negative cognitive effects. Fluoride impairs brain development. Children living in areas with higher amounts of fluoride in the water are 5 times more likely to have low IQ compared to those that do not. Studies show reduced IQ at fluoride levels as low as 0.3ppm (most public water supplies use 1ppm fluoride). Studies also show an association between fluoride exposure and visual-spatial organization. The Environmental Protection Agency (EPA) lists fluoride as one of about 100 chemicals for which there is substantial evidence for developmental neurotoxicity. Animal experiments show that fluoride damages the brain and causes learning and behavior problems. They say these experiments were done with fluoride levels that mimic the public water supply, not at very high doses.

Finally, they claim exposure to higher levels of fluoride in drinking water is linked to higher rates of osteosarcoma in boys.

These were the top health concerns I found in a brief internet search. Additional concerns also exist such as decreased freedom (being forced to drink water with fluoride), a concern that fluoride is an industrial waste product being disposed of in the water, and the belief that its safe use in rat poison allowed it to dodge FDA restrictions.

Organizations claiming fluoridation is safe and beneficial:

Now, let’s take a closer look at why some public agencies (including the American Academy of Pediatrics (AAP), American Dental Association (ADA), Centers for Disease Control and Prevention (CDC), US Public Health Service, and National Research Council) think adding fluoride to the water is beneficial and how they attempt to refute the opposition.

These agencies maintain that fluoride is good for teeth and prevents tooth decay. They say there is no scientifically valid evidence to show that it causes any serious health problems.

They do admit one possible problem resulting from too much fluoride. This is a cosmetic condition known as dental fluorosis which causes discolored patches on teeth. It occurs when young children consume too much fluoride over an extended period of time while their teeth are still growing. They state that fluoride in the U.S. water supply does not typically cause fluorosis because levels are not high enough. Fluoridated water is safe for babies and children, but there is a risk of mild fluorosis if mixing fluoridated water with infant formula or if children frequently swallow fluoridated toothpaste.

Some other arguments they make include:

The fluoride added to drinking water is regulated for safety by the Environmental Protection Agency (EPA) and it is not a by-product of the fertilizer industry.

American IQ scores have risen alongside water fluoridation. A report suggesting fluoride could impair brain development was a review of older studies that included IQ scores of children in China, Mongolia, and Iran. The study did not test cause and effect. The water in these regions had natural fluoride which was up to 10 times higher than the levels used in US public water systems.

Comparing fluoridated and non-fluoridated communities shows that fluoride is really effective at preventing tooth decay.

Fluoridated water is safe for plants, animals and fish. Fluoride occurs naturally in many bodies of fresh water and the average fluoride level in ocean water is much higher than in public water systems.

The American Cancer Society does not take an official position, but they state the following: More than 50 population-based studies have looked at the potential link between water fluoride levels and cancer. Most of these have not found a strong link to cancer.

The US Public Health Service states: Optimal fluoridation of drinking water does not pose a detectable cancer risk to humans as evidenced by extensive human epidemiological data available to date.

The National Research Council (NRC) states: “The weight of the evidence from the epidemiological [population-based] studies completed to date does not support the hypothesis of an association between fluoride exposure and increased cancer risk in humans.”

Follow-up Questions

Is there a safe amount of fluoride? When does it become unsafe?

Does fluoride add up from the drinking water, toothpaste, mouthwash, etc?

Is it better or worse to get fluoride from one source or another? (water v. toothpaste)?

Peer Reviewed Research

For this article, I conducted 10 different searches. The first one was a more generalized search of meta-analyses. These included mostly population studies to show how fluoride has affected large groups of people over time. Then, I went back and searched for evidence linking fluoridation to each adverse health claim cited by opponents. As usual, I’ve included the titles and links to all the research with brief synopses of each. You can read them or simply skip to the next section by clicking here.

Search 1: search term “fluoride”, literature reviews and meta-analyses published within the last 5 years, citing research done on humans.

1. Fluoride in drinking water and diet: the causative factor of chronic kidney diseases in the North Central Province of Sri Lanka. https://www.ncbi.nlm.nih.gov/pubmed/25916575 (2015)

This literature review provides good evidence that naturally occurring fluoride in Sri Lanka has caused chronic kidney disease. The fluoride levels in the water here are known to be excessive. People develop kidney disease over time by drinking the water and eating food made from the ground water.

2. Fluoride toothpastes and fluoride mouthrinses for home use. https://www.ncbi.nlm.nih.gov/pubmed/24308396 (2013)

Fluoride toothpastes and mouthrinses have been developed and extensive testing has demonstrated that they are effective and their use should be encouraged. Concentrations of fluoride (F), commonly found, are 1500 ppm for toothpastes and 225 ppm for mouthrinse. Several systematic reviews have concluded that fluoride-containing toothpastes and mouthrinses are effective, and that there is added benefit from their use with other fluoride delivery methods such as water fluoridation.

3.Water fluoridation and oral health. https://www.ncbi.nlm.nih.gov/pubmed/24308393 (2013)

Millions of people consume fluoridated water. Fluoride can help reduce the number of cavities and re-mineralize tooth enamel. A large number of studies conducted worldwide demonstrate the effectiveness of water fluoridation. Systematic reviews of the safety and efficacy of water fluoridation attest to its safety and efficacy; dental fluorosis identified as the only adverse outcome.

4.Milk fluoridation for the prevention of dental caries. https://www.ncbi.nlm.nih.gov/pubmed/24308395 (2013)

This lit review evaluates several RCTs and other controlled studies and shows that milk fluoridation is also an effective way to prevent cavities, especially in children with school milk programs.

5. Fluoride use in caries prevention in the primary care setting. https://www.ncbi.nlm.nih.gov/pubmed/25157014 (2014)

This review goes over the evidence showing that fluoride decreases dental caries and encourages pediatricians to use fluoride treatments in the primary care setting. It also discusses the possibility of enamel fluorosis if fluoride levels are too high.

6. Salt fluoridation and oral health. https://www.ncbi.nlm.nih.gov/pubmed/24308394 (2013)

This review shows that salt fluoridation is also effective in preventing dental caries and has been successfully implemented in parts of Europe and Latin America.

7.Exposure to fluoride in drinking water and hip fracture risk: a meta-analysis of observational studies. https://www.ncbi.nlm.nih.gov/pubmed/26020536 (2015)

Fourteen observational studies involving thirteen cohort studies and one case-control study were included in this meta-analysis. Researchers found that exposure to fluoride in drinking water does not significantly increase the incidence of hip fracture.

8. Focus on fluorides: update on the use of fluoride for the prevention of dental caries. https://www.ncbi.nlm.nih.gov/pubmed/24929594 (2014)

This review reiterates the effectiveness of water fluoridation and fluoride treatments. However, it also discusses new recommendations to reduce the amount of fluoride children are exposed to as not to cause dental fluorosis.

9. Water fluoridation: a critical review of the physiological effects of ingested fluoride as a public health intervention. https://www.ncbi.nlm.nih.gov/pubmed/24719570 (2014)

This article states that water fluoridation is controversial because it has the potential to cause major health problems while only having a modest dental caries prevention effect. The author notes that fluoride is a waste product of aluminum, fertilizer and iron ore manufacture and should not be discharged into the environment. The author argues that “systemic fluoride ingestion” should not be used to improve dental health.

10. Does cessation of community water fluoridation lead to an increase in tooth decay? A systematic review of published studies. https://www.ncbi.nlm.nih.gov/pubmed/27177581 (2016)

This review found 15 instances of communities that once had fluoridated water, but then stopped their programs. The authors state results were somewhat mixed, but overall, people got fewer cavities during the time period when the water was fluoridated.

Search 2: search terms “fluoride” and “skeletal fluorosis”, any relevant studies published within the last 5 years using human subjects

11. A brief review on experimental fluorosis. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24050947

This entire abstract is worth reading. The article reviews many harmful effects that can occur from consuming too much fluoride. I did not have access to full text.

Fluoride (F) is a naturally occurring contaminant in the water. F is essential for normal maintenance of teeth and bones. However, prolonged exposure to high concentration of F is found to be deleterious to teeth, bones and other organs. Besides drinking water, F can enter the body through food, dental products, drugs and industrial emission. People living in areas where F contamination is much higher than the expected level, are found to suffer from not only teeth and bone problem but also other systems, including brain and its functions. Since animals respond to the toxic effects of F like human beings, the deleterious effects of F have been produced experimentally in animals in order to determine the mechanism involved in the action of F. The reports indicating the chronic harmful effects of F in teeth, bones, heart, liver, kidneys, gastrointestinal tract, lungs, brain, blood, hormones and biochemical parameters of experimental animals and in in vitro studies have been reviewed in this article. The neurotoxic action of F that produces chiefly learning and memory impairment has also been included. The review also points out the harmful effects of F on reproduction, its teratogenic action and in inducing premature ageing. Finally, the reports indicating a reversal of certain toxicities of F in experimental animals after withdrawal of its exposure has been included.

12. Modifying Role of GSTP1 Polymorphism on the Association between Tea Fluoride Exposure and the Brick-Tea Type Fluorosis. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26046522

Brick tea type (skeletal) fluorosis is a public health concern in the north-west area of China. This tea is made from tea leaves which retain most of the fluoride present in the surrounding air and soil. This problem is not due to public water fluoridation or dental treatments. Researchers found that genes may play a role in the severity of fluorosis one develops from drinking this tea.

13. Association of Temporomandibular Joint Signs & Symptoms with Dental Fluorosis & Skeletal Manifestations in Endemic Fluoride Areas of Dungarpur District, Rajasthan, India. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26816986

Endemic fluorosis resulting from high fluoride concentration in groundwater is a major public health problem. India is among the numerous nations, where fluoride sullied groundwater is creating wellbeing issues. This study found that TMJ was also associated with dental and skeletal fluorosis in India.

14. Prevalence of skeletal fluorosis in fisherman from Kutch coast, Gujarat, India. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26656421

In health terms, consuming fluoride is well recognized to be a double-edged sword. Consumption of optimal amounts is beneficial to health, however an excess constitutes a health hazard. This study found that 30% of fisherman in Kutch coast, Gujarat, India had some degree of skeletal fluorosis due to fluoride concentrations in the drinking water. The drinking water in this area was between 3.4 and 6.9 ppm.

15. Dietary Fluoride Intake and Associated Skeletal and Dental Fluorosis in School Age Children in Rural Ethiopian Rift Valley. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27472351

This study showed that children in a part of rural Ethiopia had dental and skeletal fluorosis from drinking ground water and eating food cultivated with this water. Children here were regularly consuming more than 10 mg of fluoride per day (much more than the highest acceptable dose in the US). The research also found that higher consumption of calcium and using rain water rather than ground water could reduce fluorosis in this region.

16. Study of the relationship between the lifestyle of residents residing in fluorosis endemic areas and adult skeletal fluorosis. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26183810

Excerpt from abstract:

The relationship between fluorosis and the lifestyle of adult residents of areas in which fluorosis is endemic was evaluated. Our results showed that protective factors against skeletal fluorosis included drinking boiled water, storing water in a ceramic tank, and ingesting fruits, vitamin A, thiamine, and folic acid. Risk factors for skeletal fluorosis were overweight status and obesity, drinking tea, drinking water without storage, and ingestion of oils, fats, and phosphorus.

Search 3: search terms “fluoride” and “osteoarthririts”, any relevant studies published within the last 5 years using human subjects

I found no research linking fluoridated drinking water, food, beverages or dental products to osteoarthritis. A search of “fluoride” + “osteoarthritis” yielded results showing that a certain type of PET scan (18F-fluoride PET) can be used to evaluate hip osteoarthritis. These studies are irrelevant to our questions because they do not involve consumption of fluoride in the daily diet.

Search 4: search terms “fluoride” and “thyroid”, any relevant studies published within the last 5 years using human subjects

17. The effects and underlying mechanism of excessive iodide on excessive fluoride-induced thyroid cytotoxicity. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25104093

This study found that excessive amounts of fluoride can damage human thyroid cells. It also found that excessive iodide is often found with excessive fluoride. This can cause further thyroid damage. I did not determine exactly how much they considered to be “excessive”, but this study does seem to be referring to excessive fluoride and iodide in ground water and not public water systems in which fluoride has been added.

18. Public perceptions and scientific evidence for perceived harms/risks of community water fluoridation: An examination of online comments pertaining to fluoridation cessation in Calgary in 2011. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26680434

This study looked at public concerns about fluoridation. It found that people are concerned about the effect of fluoride on their health, the environment, and animal health. However, evidence people cited was weak and typically included anecdotes and what they considered to be expert opinions. The authors stated that when they searched the literature, they did find evidence of harm to the thyroid and to phytoplankton at levels exceeding 1.5 ppm (the current recommendation is 0.7ppm).

19. Fluoride exposure and indicators of thyroid functioning in the Canadian population: implications for community water fluoridation. (2017) https://www.ncbi.nlm.nih.gov/pubmed/28839078

This study analyzed data from a large population in Canada that gets fluoridated water. They found no association between fluoride (from community water systems and toothpaste/mouthwash) and thyroid dysfunction or abnormal levels of thyroid stimulating hormone.

20. Dental fluorosis, nutritional status, kidney damage, and thyroid function along with bone metabolic indicators in school-going children living in fluoride-affected hilly areas of Doda district, Jammu and Kashmir, India. (2017) https://www.ncbi.nlm.nih.gov/pubmed/29063198

This study included 824 children age 8-15. Half were from an area with high levels of fluoride in the ground water and half were not. In children from the high fluoride area, they found fluorosis, chronic kidney damage and decreased thyroid stimulating hormone. I was unable to determine exactly how much fluoride was in the water in the high-fluoride area.

Search 5: search terms “fluoride” and “pineal gland”, any relevant studies published within the last 10 years using human subjects

21. Fluoride deposition in the aged human pineal gland. (2001) https://www.ncbi.nlm.nih.gov/pubmed/11275672

The purpose of this study was to discover whether fluoride accumulates in the aged human pineal gland. Cadaver studies were performed. They found that by old age, the pineal gland has readily accumulated fluoride and its fluoride to calcium ratio is higher than bone.

Search 6: search terms “fluoride” and “puberty”, any relevant studies published within the last 10 years using human subjects

No studies found investigating whether fluoride causes early puberty.

Search 7: search terms “fluoride” and “fertility”, any relevant studies published within the last 5 years using animal subjects (no relevant studies on human subjects found)

22. The toxicity mechanism of sodium fluoride on fertility in female rats. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24071475

This study showed that high levels of fluoride in drinking water (100-200mg/liter) caused reductions in reproductive hormones and problems with related receptor proteins in female rats. (keep in mind, the recommended amount of fluoride in public drinking water is 0.7mg/liter).

23. Effect of sodium fluoride on male mouse fertility. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25854509

This study found that high concentrations of sodium fluoride could impair mouse sperm’s motility and ability to fertilize an egg in vitro (outside the body).

24. Sodium fluoride activates ERK and JNK via induction of oxidative stress to promote apoptosis and impairs ovarian function in rats. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24681588

This study also tested female rats who had received 100-200 mg/liter of fluoride in their drinking water. They found that the fluoride caused ovarian cell death caused by oxidative stress.

25. Toxic effects of sodium fluoride on cell proliferation and apoptosis of Leydig cells from young mice. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25074826

This study found similar results to the one above, but went into more detail about the mechanisms of cell death caused by high levels of fluoride.

26. Adverse Effects of High Concentrations of Fluoride on Characteristics of the Ovary and Mature Oocyte of Mouse. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26053026

This study found similar results to the studies above.

27. Effects of sodium fluoride on reproductive function in female rats. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23459146

Again, this study also found reduced fertility in female rats that had been exposed to high levels of fluoride. They also found that it damaged the structure of the uterus.

Search 8: search terms “fluoride” and “IQ”, any relevant studies published within the last 5 years using human subjects

28. A cross-sectional study to assess the intelligence quotient (IQ) of school going children aged 10-12 years in villages of Mysore district, India with different fluoride levels. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26381633

This study found that children in India whose water contained high levels (2.2mg/liter) of fluoride had lower IQs than children who drank water with less fluoride (1.2mg/liter or less).

29. Dental fluorosis and urinary fluoride concentration as a reflection of fluoride exposure and its impact on IQ level and BMI of children of Laxmisagar, Simlapal Block of Bankura District, W.B., India. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26960765

This study found that dental fluorosis and urinary fluoride was negatively associated with IQ in children in India whose drinking water had approximately 2.11 mg/liter of fluoride.

30. Inferring the fluoride hydrogeochemistry and effect of consuming fluoride-contaminated drinking water on human health in some endemic areas of Birbhum district, West Bengal. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26164468

This study found correlations between children with fluorosis and lower IQs in West Bengal. The amount of fluoride in drinking water in this area varies from 0.33 to 18.08 mg/liter.

31. Prenatal Fluoride Exposure and Cognitive Outcomes in Children at 4 and 6-12 Years of Age in Mexico. (2017) https://www.ncbi.nlm.nih.gov/pubmed/28937959

This study found that high prenatal fluoride exposure was associated with lower scores on IQ tests in children at ages 4-12. I was unable to determine the amount of fluoride in the water that was considered “high” in this study.

32. Fluoride exposure and reported learning disability diagnosis among Canadian children: Implications for community water fluoridation. (2017)  https://www.ncbi.nlm.nih.gov/pubmed/28910243

This study found no link between fluoride exposure and lower IQ or other cognitive diagnoses in children in Canada. Researchers here, like in other studies, used urinary fluoride to determine levels of fluoride consumption. However, they also used “creatine-adjusted urinary fluoride” which the authors stated provides a more accurate measurement. I was unable to determine the exact amounts of fluoride in the Canadian drinking water.

Search 9: Search terms “fluoride” and “osteosarcoma” (bone cancer), any relevant studies published within the last 5 years using human subjects

33. Is fluoride a risk factor for bone cancer? Small area analysis of osteosarcoma and Ewing sarcoma diagnosed among 0-49-year-olds in Great Britain, 1980-2005. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24425828

This study examined 2,566 cases of bone cancer in Great Britain. Researchers found no association between higher levels of fluoride in the water and bone cancer.

34. Fluoride exposure in public drinking water and childhood and adolescent osteosarcoma in Texas. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27189068

This study looked at 308 cases of osteosarcoma in children and adolescents in Texas between 1996 and 2006. They also had a control group of children diagnosed with leukemia or CNS tumors. Researchers found no association between fluoride levels in public drinking water and bone cancer.

35. Community water fluoridation and health outcomes in England: a cross-sectional study. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26153549

This study looked for associations between fluoride and a number of health outcomes in areas in England with public water fluoridation. They found strong evidence that fluoridated water reduces dental caries in children. There was no evidence of an association between fluoride and hip fracture, Down syndrome, all-cancer, all-cause mortality or osteosarcoma. Bladder cancer and renal stones were negatively associated with fluoridation.

Search 10: Search terms “fluoride” and “heart disease”, any relevant studies published within the last 5 years using human subjects

36. Natural fluoride in drinking water and myocardial infarction: A cohort study in Sweden. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27100011

This study looked at 455,619 individuals born in Sweden between 1900 and 1919. They were divided into groups based on the amount of fluoride in their drinking water. Groups ranged from <0.3 mg/liter to >1.5mg/liter. Myocardial infarction (heart attack) was not associated with water fluoride levels for any of the groups.

What We Know and Don’t Know

From on my search of meta-analysis and literature reviews, 7 out of 8 articles supported water, salt, or milk fluoridation. Thousands of people were studied over time and people who ingested small amounts of fluoride had about 50% fewer cavities than those who did not. However, the rate of cavity reduction varied throughout the literature from 15-60%.

The only adverse health effect seen in these studies was dental fluorosis in young children. Some of the studies recommended reducing overall fluoride for children by using non-fluoridated water in infant formula or by using non-fluoridated toothpastes for very young children who may swallow it.

One review stood out from the others by claiming fluoridated water is more harmful than beneficial. The authors cite evidence that topical fluoride is effective in reducing cavities, but ingested fluoride is not. They cite research questioning the safety of moderate doses of fluoride and show how fluoride consumption can add up easily depending on what/how much a person eats or drinks.

In my first search, I also came across one meta-analysis that looked at hip fractures. It found that hip fractures were not linked to fluoridated water. Another meta-analysis looked at kidney disease in an area with very high levels of ground water fluoride. This study found a clear link between fluoride and kidney disease.

The second search I did focused on skeletal fluorosis, which is a painful condition caused by fluoride accumulating in the bones and joints. I found 6 relevant articles, all of which confirmed that too much fluoride causes skeletal fluorosis. These studies were done in developing nations with ground fluoride levels around 3-7ppm. They also discovered some genetic predisposition to fluorosis.

The third search yielded no results linking fluoride to osteoarthritis.

Search 4 evaluated the effects of fluoride on the thyroid. Across studies, thyroid damage was found in areas of high fluoride ground water, but not in areas that added small amounts of fluoride to drinking water.

Search 5 confirmed that fluoride does accumulate in the pineal gland over time. No adverse effects were discussed in the cadaver study article I found. No other research was found linking fluoride consumption to pineal gland damage.

Search 6 yielded no results linking fluoride consumption to early puberty.

In search 7, I found a wealth of literature linking high levels of fluoride to fertility problems in mice. However, the mice studied consumed about 100-200 times recommended the amount of fluoride. Fertility problems were consistently found in both male and female mice.

Search 8 evaluated the link between fluoride and child IQ. Again, I found several studies correlating high levels of fluoride in ground water in developing countries to lower IQ. Levels of fluoride in these studies varied widely (up to 18 times the recommended amount).

For search 9, I found 3 robust studies looking at community water fluoridation and rates of osteosarcoma. No study found any associations. These studies were done in developed countries who purposefully fluoridated their water supply.

Finally, search 10 evaluated a link between fluoride and heart attack. I found one study which was from Sweden. No link was found.

To summarize, here is what we know:

Many developing countries drink well water that has fluoride concentrations 2-18 times the recommended concentration. There are well-established health risks to consuming these larger amounts of fluoride. These include skeletal fluorosis, kidney disease, thyroid damage, impaired brain development, and possibly decreased fertility.

Other countries drink water containing around 0.7ppm fluoride. This amount of fluoride is strongly correlated with reduced dental caries, especially in children. Fluoride works in 2 ways to reduce cavities. First, it works by strengthening teeth from the inside while they are forming. Second, it works by helping to reduce bacteria and improve the rebuilding of enamel when applied topically.

At fluoride concentrations between 1-2 ppm, some children will develop dental fluorosis, or discoloration of teeth. This is the first sign that a child may be receiving too much fluoride. This can also happen if a child regularly swallows toothpaste or mouthwash.

To answer my follow-up questions, yes there is a point where fluoride levels go from beneficial to detrimental. It seems like the greatest benefits are between 0.7 and 1.0ppm while mild adverse effects start to occur around 2ppm. Fluoride does add up from all sources. Dentists recommend both ingested and topical sources, but we should keep in mind that these add up. This is the main reason community water supplies were reduced from 1 to 0.7ppm. I was unable to find data regarding whether ingested or topical fluoride is safer or more effective. One thing to consider is that ingested fluoride actually acts topically by simply being present in saliva.

Conclusions and Applications

Based on my research, community water fluoridation is safe. It prevents about a quarter to half of dental caries in the general population. People who drink well water, especially in developing nations, are at risk for several serious health problems. People who drink from the public water supply in the U.S. are not.

My recommendation is not to worry about the fluoride in your water. If you are concerned about your children developing dental fluorosis, consider limiting their exposure. Make sure they don’t swallow fluoride toothpaste and consider alternating fluoridated and non-fluoridated water sources.

What about Saturated Fat?

Now that dairy has been vindicated, let’s take a look at another highly controversial dietary component: saturated fat.

Here’s a brief review of the debate which began back in the 1950’s.

By the mid-20th century, heart disease had become the leading cause of death in the US. President Eisenhower had a heart attack which brought the heart disease issue to the forefront of the country’s focus. Researchers learned that cholesterol was a component in the plaques that block peoples’ arteries. They knew that dietary saturated fat (fat that comes mostly from animals and tropical oils) could increase the amount of cholesterol in peoples’ blood. Therefore, they hypothesized that saturated fat raised cholesterol in the blood which then formed plaques in the arteries which then caused heart attacks.

Nutrition researcher Ancel Keys published a now infamous study which claimed that men in countries that ate more saturated fat had much more heart disease than men in countries that ate less saturated fat. The United States Department of Agriculture (USDA) then published guidelines encouraging people to eat fewer than 10% of calories from saturated fat.

In recent decades, Keys’ study has been criticized for only reporting data on countries that supported his hypothesis. Some other studies have not been able to replicate his findings. Furthermore, we now have a better understanding of how different types of cholesterol work in the body and how other nutrients may contribute to heart disease. These 3 issues have raised controversy over whether saturated fat should continue to be limited in a healthy diet.

Initial Google Search

Most mainstream organizations such as the USDA and American Heart Association (AHA) continue to recommend reducing dietary saturated fat to 5-10% of total calories. These claims come directly from the AHA:

  • Eating foods that contain saturated fats raises the level of cholesterol in your blood. High levels of LDL cholesterol in your blood increase your risk of heart disease and stroke.
  • Decades of sound science has proven it can raise your “bad” cholesterol and put you at higher risk for heart disease.
  • Eleven authoritative bodies – including the World Health Organization; the Institute of Medicine; the governments of the United States, the United Kingdom; and the European Union – independently reviewed the scientific evidence (through November 2017) and concluded yet again that saturated fat is associated with heart disease.
  • Research shows that a diet rich in refined, simple carbohydrates is equally if not more detrimental to health than a fatty diet.
  • Not all fats are created equal. Saturated fats increase risk for heart disease, but that’s not the case with unsaturated fats known as monounsaturated and polyunsaturated fats. These fats are found in fish, nuts, seeds and oils from plants. However, it’s important to remember that unsaturated fats do contain calories. And too many calories can lead to weight gain. Still, unsaturated fats are generally better.

Groups and individuals that question these recommendations cite the following:

  • Saturated fats raise both LDL (cholesterol that can clog arteries) and HDL (cholesterol that clears away clogs in arteries) resulting in a net balance effect. Therefore, total cholesterol is not a good indicator of risk.
  • There are even different types of LDL. The smaller LDL particles are more likely to become oxidized and clog arteries while the larger LDL particles are less likely. Smaller LDL particles increase due to carbohydrate consumption. Larger LDL particles increase due to saturated fat. Therefore, carbs are more likely to cause heart disease than animal fat.
  • Correlation is not causation. Countries with higher saturated fat consumption may have more heart disease, but these same countries also have higher sugar consumption. Sugar may be more dangerous than saturated fat.
  • Many other studies and meta-analyses have found that saturated fat consumption does not affect heart disease risk.
  • Using polyunsaturated fats as a replacement for saturated fats may lower LDL, but they also lower HDL.
  • Non-saturated fats oxidize more easily when heated (during cooking) and in the body which causes inflammation and heart disease.
  • Polyunsaturated fats are primarily omega-6 fatty acids which increase inflammation when not balanced out by omega-3 fatty acids.
  • The AHA and other similar guidelines may be based on cherry-picked or poorly interpreted data.

Of note, both sides equally agree that trans fats (hydrogenated and partially hydrogenated oils) cause more harm than any other kind of fat.

After reading both sides of the argument, I really don’t know which way to lean. Luckily, tons of high quality research has been done on this topic.

To find relevant research, I used the following inclusion criteria: saturated fat (search term), heart or cardiovascular disease outcomes, literature reviews or meta-analysis, done within past 5 years, access to full text in English.

I found 14 relevant literature reviews and meta-analyses from the past 5 years that met all the criteria and compiled them here. In order to make sense of the findings, we must be familiar with two important types of research design: randomized controlled trials and prospective cohort studies.

A randomized controlled trial (RCT) is a study in which people are allocated at random either to receive the clinical intervention being tested or to be a part of the control group that will receive either no intervention or the standard intervention (not the new intervention being tested). RCTs provide the most reliable type of evidence. You can usually say that something happened as a result of the intervention without wondering whether another factor was at play. With RCTs you can be more sure that X caused Y and not just that X is associated with Y.

The second most common type of study in the research below is the prospective cohort study (PCS). These studies follow a large group of people over a long time to determine how their behaviors or characteristics affect certain outcomes. These studies can give us a lot of good information, but they cannot let us say for sure that X caused Y. We can only say that X is associated with Y. This leaves room for cofounding variables that may have been the real cause of Y.

A few other terms should be identified in order to make sense of the rest of this blog. Here they are:

  • Saturated fatty acid (SFA): fat molecules that have no double bonds. These fats are solid at room temperature. They are found mainly in meat, dairy and tropical oils.
  • Monounsaturated fatty acid (MUFA): fat molecules that have one double bond. They are liquid at room temperature and are found mainly in olive oil, olives, avocados, nuts, sunflower oil, sesame oil, and animal products.
  • Polyunsaturated fatty acid (PUFA): fat molecules that have more than one double bond. They are liquid at room temperature and found in nuts, seeds, fish, seed oils and oysters. Depending on where the first double bond lies, they are classified as either omega-3 or omega-6.
  • Cardiovascular disease (CVD): catch all term for any cause of heart disease, usually caused by damaged blood vessels.
  • Coronary heart/artery disease (CHD or CAD): heart disease involving the heart’s major blood vessels
  • Low density lipoprotein (LDL): protein that carries cholesterol through the body. LDL cholesterol is known as the “bad cholesterol” because it can build up on the walls of blood vessels and cause heart disease. LDL comes in various sizes. The smaller the particles, the more likely they are to stick to the blood vessels.
  • High density lipoprotein (HDL): protein that carries cholesterol to the liver and out of the body. HDL is known as the “good cholesterol”.
  • American Heart Association (AHA): large non-profit organization providing research and guidelines on how to reduce heart disease and stroke.
  • United States Department of Agriculture (USDA): government program responsible for developing laws related to farming, forestry and food.
  • Randomized Controlled Trial (RCT) See above
  • Prospective Cohort Study (PCS) See above

The research below begins with the AHA guidelines because this document is the most influential driver of USDA policy. The other research either aligns with this article or attempts to show that it is fully or partially inaccurate. So, let’s take a closer look.

Peer Reviewed Research (Click here to skip the research and go straight to the conclusions)

1. Dietary Fats and Cardiovascular Disease: A Presidential Advisory From the American Heart Association. (2017) https://www.ncbi.nlm.nih.gov/pubmed/28620111

This article relies heavily on 4 high quality randomized controlled trials conducted in the 1960s that directly measure replacing saturated fat with polyunsaturated fat over the course of at least 2 years. These 4 trials had important inclusion criteria. They did not include trans-fat as a major component, they controlled the dietary intake of both the test and control groups, the proved adherence to the diet by using biomarkers, and they collected information on cardiovascular or coronary disease events.

It also discusses 6 other randomized controlled trials that replaced saturated fat with nonsaturated fat, but may not have met other the other criteria. There have been no randomized controlled trials that replaced saturated fat with whole grains, fruits and vegetables instead of nonsaturated fat and no randomized controlled trials that purposefully replaced saturated fat with refined carbohydrates. There have also been no more recent randomized controlled trials that fit the criteria.

All 10 of these randomized controlled trials found that replacing saturated fat with nonsaturated fat resulted in a decrease in CVD and that LDL was lowered an average of about 30% (which is about the same as we would expect from a statin drug). The article goes on to show through meta-regression analysis that reductions in LDL cholesterol after diet change correlate well with the extent of reductions in CVD. They discuss “very strong evidence that satisfied rigorous criteria for causality” which means there is very high quality evidence leading us to believe that high LDL indeed causes CVD and that lowering LDL indeed lowers CVD.

The article also cites several other interesting studies showing that different types of saturated fat make little difference. Coconut oil and dairy fat did not have protective benefits and seemed to be similar to any other saturated fat in terms of CVD.

Additionally, they cite a study showing that consumption of saturated fat reduces the anti-inflammatory potential of HDL. This would mean that even though saturated fat raises both good and bad cholesterol, it makes the good cholesterol not work as well.

The authors identify what they say is the main reason why some meta-analyses found different results. Prospective cohort studies of PCSs (as opposed to randomized controlled trials) generally saw participants replacing saturated fat with packaged low-fat foods (refined carbohydrates). These studies found that reducing saturated fat was not associated with reducing CVD. Some of them even saw a rise in CVD. The AHA readily acknowledges that saturated fat should not be replaced with refined carbohydrates.

2. Fat, Sugar, Whole Grains and Heart Disease: 50 Years of Confusion. (2018) https://www.ncbi.nlm.nih.gov/pubmed/29300309

This article does not deny the findings from the studies in the AHA article, but it places much stronger blame on refined carbohydrates than SFAs. The review cites PCSs that show the association between saturated fat and CHD is present, but weak. The author confirms that RCTs show that increasing PUFAs while decreasing SFAs will lower the ratio of total cholesterol to HDL, lower triglycerides, and reduce CHD. However, he cites evidence suggesting that these RCTs may have been poorly controlled and less reliable than we once thought. He emphasizes that PCSs show a strong association between sugar/refined carbohydrates and CHD. He also stresses that fruits, vegetables, fish, and whole grains are inversely associated with CHD (protective against heart disease).

3. Reduction in saturated fat intake for cardiovascular disease. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26068959

This meta-analysis looked at whether it is best to replace SFAs with PUFAs, MUFAs, carbohydrates or protein. They included only randomized controlled trials. The researchers found the strongest decrease in CHD when SFAs were replaced with PUFAs. Their findings align well with the AHA guidelines. This analysis did not find any reduction in CHD when SFAs were replaced by carbohydrates or protein, but it did not specify carbohydrate type. They stated that the evidence for MUFAs was inconclusive due to only one trial including them. Overall, this review is very similar to the AHA review and had similar conclusions.

4. Saturated Fats Versus Polyunsaturated Fats Versus Carbohydrates for Cardiovascular Disease Prevention and Treatment. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26185980

This literature review is similar to the study 2 above. The authors start by acknowledging that replacing SFAs with PUFAs, especially omega-3’s, seems to improve cardiovascular health in several RCTs. They also state that when SFAs are replaced by carbohydrates, there is either no change, or a decrease in cardiovascular health. They cite other health problems caused by refined carbs and sugars and agree with the US Dietary Guidelines of limiting added sugars to less than 10% of calories per day. They say that urging people to eat only 5% of calories from SFAs may lead people to eat more sugar, so they tend to agree with the past recommendation of 10% of calories from SFAs.

The authors describe how fats and carbohydrates act differently in the body. SFAs increase large LDL whereas refined carbohydrates increase small LDL. The small LDL particles are more strongly associated with CVD than the large ones.

This study also looks at how different foods with SFAs act differently in the body. They cite research suggesting that dairy fat does not raise LDL the same way other sources of saturated fat might. They acknowledge that beef is associated with CVD, but that this may be attributed to another factor, carnitine-derived metabolites, rather than SFAs. They cite evidence that butter, palm oil and coconut oil do raise LDL, but perhaps not as much as we would predict given the specific types of fatty acids they are made of.

They also discuss how weight loss is the key factor to improving cardiovascular health no matter which macronutrients you eat. They conclude that overall dietary patterns are more important than focusing on specific macronutrients or fatty acids. They emphasize vegetables, fish, nuts and whole grains. Their overall tone is that the effect of SFAs on heart disease has not been well established.

5. Intake of saturated and trans unsaturated fatty acids and risk of all cause mortality, cardiovascular disease, and type 2 diabetes: systematic review and meta-analysis of observational studies. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26268692

From reading the abstract, this review seems to refute the AHA’s claim that replacing SFAs with PUFAs will reduce CVD. However, from the title, we can see that this review only includes observational studies. That means they used prospective cohort studies and not randomized controlled trials. We can also see that they studied trans fats which are already known to increase CVD. Upon reading the details, the PCSs cited here saw people swapping out saturated fat for refined grains and sugar, just as the AHA article pointed out. So, upon further examination, this review actually doesn’t claim that replacing saturated fat with nonsaturated fat doesn’t help. It only claims that replacing saturated fat with refined carbohydrates doesn’t help. These findings really aren’t different from the AHA claims.

6. The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26586275

This review makes the claim that sugar (especially fructose) is more likely to cause CVD than saturated fat. As we now know, this is not in contrast with the AHA guidelines. This review also cites studies that suggest certain types of saturated fat may be protective to the heart by increasing HDL or large LDL particles. There still seems to be debate over whether this is true. By the end of the review, the authors are simply urging people to eat more real food and “living botanical plants” rather than replacing saturated fats with highly processed foods. They wish the AHA would also concentrate on foods instead of individual fatty acids.

7. Dietary Fat and Risk of Cardiovascular Disease: Recent Controversies and Advances. (2017) https://www.ncbi.nlm.nih.gov/pubmed/28645222

This review reiterates what we’ve already seen. Replacing SFAs with PUFAs will decrease LDL significantly. Replacing SFAs with refined carbohydrates does not. Replacing SFAs with whole grains decreases LDL slightly. They cite two PCSs that associate dairy fat with reduced CVD risk, but then cite 3 PCSs where dairy fat was replaced by PUFAs. Replacing dairy fat with PUFAs was associated with decreased CVD risk. Another RCT found that CVD was reduced when butter was replaced by vegetable oil and full fat milk was replaced by skim milk with a vegetable oil emulsion.

Importantly, this review cites several studies refuting the claim that omega-6 PUFAs lead to inflammation. They explain how PUFAs break down in the body and are not associated with a net increase in any inflammatory markers. They cite many studies showing that omega-3 PUFAs (mainly from patients eating fatty fish) decrease inflammation and CVD risk, but the evidence on fish oil supplementation was inconclusive. The review also cites evidence showing beneficial effects of MUFAs (mainly from nuts and olive oil) on LDL and CVD. Overall, this review matches the AHA recommendations.

8. Dietary fats and health: dietary recommendations in the context of scientific evidence. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23674795

This literature review is written by Glen D. Lawrence, author of “The Fats of Life”. Although his article does not discuss any RCTs, he presents convincing arguments that sugar is primarily to blame for the rise in heart disease and several other diseases including cancer and diabetes. This alone does not stand in contrast to the AHA claims. He admits that SFAs increase LDL, but stresses that they also raise HDL. Lawrence cites data supporting positive health effects of dairy fat and coconut oil and stresses the importance of high quality non-processed meats. The majority of his article discusses polyunsaturated fatty acids (PUFAs) which are what the AHA would claim to be the “good” kid of fats. He cites research claiming that PUFAs are susceptible to oxidization whereas SFAs are not. These oxidized particles (from PUFAs and carbohydrates) are what really cause atherosclerosis and inflammation. He claims that cooking meats at high temperatures causes oxidation of the PUFAs in the meat which then causes heart disease (and cancer) rather than the SFAs in the meat. He also argues that omega 3 PUFAs help mitigate the harm done by omega 6 PUFAs. To simplify, Lawrence’s article argues that SFAs from natural sources are healthy in moderate quantities, and that omega 6 PUFAs and sugar are causing heart disease.

9. It is time to revisit current dietary recommendations for saturated fat. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25293492

This review attempts to point out flaws in the current AHA recommendations. They state that the impact of SFA on blood cholesterol is undisputable, but the resulting impact on CVD risk is not as straight-forward which has caused people to misinterpret data. They cite research showing that SFAs increase the large LDL particles and SFAs reduce triglycerides better than carbohydrates. They also claim that the evidence regarding PUFAs and oxidation/inflammation is unclear. They point to the same research we’ve already seen that associates dairy fat with a lower risk of CHD. In sum, these authors feel that the recommendations against SFAs have ignored data to the contrary.

10. Emerging nutrition science on fatty acids and cardiovascular disease: nutritionists’ perspectives. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25979506

This review of the literature fully supports the AHA recommendations. They break down different components of saturated and unsaturated fats and describe how each affects the human body. The authors feel that the research supports replacing SFAs with PUFAs (like vegetable oil) rather than MUFAs (like olive oil). They also remind us that all oils and fat sources contain certain amounts of SFAs, PUFAs and MUFAs.

11. Evidence for and against dietary recommendations to prevent cardiovascular disease. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26175635

This author of this review discusses how some SFAs may be beneficial. For example, she states that lauric acid (high in dairy and tropical oils) has a favorable impact on the total cholesterol to HDL ratio and that stearic acid (high in beef tallow and cocoa butter) has no effect on cholesterol. She also questioned why the AHA guidelines only used LDL, HDL, triglycerides and blood pressure to measure outcomes and not obesity, diabetes or metabolic syndrome. She cited the difference between small and large LDL particles as we have seen in other reviews. She credited the AHA and USDA for recommending decreased sugar intake and acknowledging that processed meats are more harmful than red meats. Her conclusion emphasized the need to focus on whole foods when making recommendations rather than specific nutrients like saturated fat.

12. The relation of saturated fatty acids with low-grade inflammation and cardiovascular disease. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27692243

This review is very similar to the one above. The authors’ main argument is that SFAs are just one of many lifestyle factors that can cause heart disease. These authors come from a background of studying Paleolithic nutrition and lifestyle. They go into great detail about research questioning whether SFAs are actually responsible for heart disease. One interesting point they make is that two thirds of people admitted for “acute coronary events” suffer from metabolic syndrome, but 75% of these people have normal LDL and total cholesterol. They are questioning the importance of LDL as a risk factor. Then they go on to make the claim we have seen before that SFA increases large LDL particles, but not small ones, which truly cause CVD.

They spend much of the article discussing the importance of omega-3 PUFA and how it works synergistically with SFAs. They cite research claiming that harmful effects of SFAs are only present when omega-3 PUFAs are too low.

A few other points they make include: (1) human breastmilk contains high amounts of SFA, (2) wild animals have more MUFA and PUFA and less SFA than farm-raised animals, (3) high fat diets are better than low fat diets at improving blood pressure, HDL, triglycerides, and fasting glucose.

In the end, they call for a variety of diet and lifestyle recommendations: increased consumption of fish, vegetables, fruits, fiber, and whole grains; decreased consumption of salt, alcohol, sugar and fructose; more exercise and sleep, and less stress, anxiety, depression and pollution. These final recommendations don’t look too far off from what the AHA recommends.

13. Dietary fatty acids in the secondary prevention of coronary heart disease: a systematic review, meta-analysis and meta-regression. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24747790

This meta-analysis analyzed 21 prospective cohort studies with more than 7,000 participants who had all already had a coronary event. Some of these studies found that replacing SFA with MUFA or PUFA had favorable results while other did not find significant results. The authors found that overall, the results of dietary fat manipulation were not significant when it came to a second coronary event. However, the researchers recommended replacing SFAs with omega-3 PUFAs in their conclusion.

14. Effect of the amount and type of dietary fat on cardiometabolic risk factors and risk of developing type 2 diabetes, cardiovascular diseases, and cancer: a systematic review (2014) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4095759/

This is a systematic review that combined results from 607 studies including RCTs, PCHs and some case studies in order to figure out whether the type of fat people consumed had an effect on heart disease, diabetes and cancer. Here is a list of what they found:

Substitution of SFA with MUFA and/or PUFA decreases LDL, but there were no firm conclusions about which type (small or large LDL) was decreased.

There is convincing evidence that replacing SFA with PUFA can reduce CVD events by 10-20%.

The type of fat had no impact on body weight.

When PUFA replaced SFA or carbohydrates, the risk of type 2 diabetes was reduced.

Specific SFA from dairy may have an inverse relationship with type 2 diabetes, but results were inconclusive.

There is probable or convincing evidence linking increased body fat with most types of cancer, but the evidence linking specific types of fat with specific types of cancer is weak.

What We Know and Don’t Know

After analyzing the research, we have 4 reviews that completely align with the American Heart Association recommendations, 4 reviews that mostly align, and 5 that seem to refute the recommendations.

None of the research can deny that replacing SFA with PUFA and/or MUFA will lower LDL. The debate arises as to which type of LDL is being raised by SFA. Is it the large LDL particles that are less likely to cause heart disease, the small LDL particles which are more likely to cause heart disease, or both? There is also debate about how much LDL really matters. Some think we should focus more on triglycerides, the ratio of total cholesterol to HDL or other markers of metabolic syndrome.

These questions are not adequately answered in the research above. All we know for sure is that the RCTs (remember, this is the most reliable type of evidence) found that people had fewer coronary events (aka heart attacks) when SFA was replaced by PUFA or MUFA.

The research also consistently shows that replacing saturated fat with trans-fat or refined carbohydrates increases heart disease risk. This is probably the most important take home point, so I’ll repeat it:

Everyone agrees that refined carbohydrates increase the risk of heart disease even more than saturated fat!

Some researchers just feel that we should stop talking about SFA and only focus on reducing sugar/carbohydrate.

Some research shows that the source of the saturated fat (whole milk, butter, egg yolk, coconut oil, meat, etc.) makes little difference. However, there is still considerable debate over whether full-fat dairy could have protective effects. As we saw in my previous blog, all types of dairy have been associated with positive health outcomes.

The evidence in support of tropical oils and butter does not seem to suggest these are good for you, only that they may not be as bad as we once thought. None of the research I read specifically singled out egg yolks.

Another point of contention is oxidation and inflammation. PUFAs are the most likely type of fat to be damaged by oxidation because of their chemical structure. Some researchers argue that oxidation causes inflammation which causes heart disease. I was unable to find the AHA’s response to this claim.

Finally, some argue that the balance of omega-6 and omega-3 PUFA in approximately a 4:1 ratio is critical. Most research studies did not address this issue, but some researchers feel there is reason to believe SFAs are only harmful because people these days don’t consume enough omega-3 PUFA. Regardless of the importance of balancing types of PUFA, all the research supports consuming more omega-3 fatty acids from real foods, especially fish.

Many of the articles reviewed here stress the need to create guidelines based on actual foods rather than nutrients. Others say things like, “We should shift the focus from reducing saturated fat to reducing sugar in the diet”. In reality, the research supports reducing saturated fat AND reducing sugar/refined carbohydrates.

Conclusions and Applications

At the end of the day, all of the research I found concluded that we really should stick to vegetables, fruits, fish, lean meats, nuts, seeds, dairy, and whole grains in order to be healthy. Considering all the research together, it would seem reasonable to suggest a heart-healthy diet of 5-10% of calories from saturated fat, 5-10% of calories from sugar/refined carbohydrate (sorry alcohol is included in this category too), and as little trans-fat as possible. It would be even better to show people examples of how to eat according to these guidelines in terms of real foods.

Let’s take a look at how we might put this into practice with the typical 2,000 calorie diet. If we split the difference and have 7.5% calories from saturated fat and 7.5% calories from refined carbs, added sugar, or alcohol, we get 150 calories for each. I considered making sample menus using these guidelines, but I actually think that would make a simple message more complicated.

Many nutrition experts say you should never classify foods as “good” and “bad”. I’m going to break that rule. Based on the research I found,

Saturated fat is mostly bad for you. Sugar, refined carbohydrates, and alcohol are even worse.

All questions and comments are appreciated!


What’s the Deal with Dairy?

In the past few months, I have presented research that suggests that following either a plant based vegan or a traditional paleo diet may be better for your health than following diet recommendations of the American Heart Association or American Diabetes Association.

To review, a plant based vegan diet consists of mainly vegetables, fruits, whole grains, legumes, nuts, and seeds. A traditional paleo diet includes mainly vegetables, some fruit, lean meats, eggs, nuts, and seeds. The vegan diet excludes meat and eggs while the paleo diet excludes grains. Both diets exclude dairy, processed foods, added sugar, and most saturated fat (some versions of the paleo diet include high amounts of saturated fat that are not typical of the more traditional paleo diet usually used in research studies). Meanwhile, the recommended diets of most mainstream nutrition groups include all of the foods in the vegan and paleo diets plus low-fat dairy, but still exclude processed foods, added sugar, and saturated fat.

The key food that is excluded from the paleo and vegan diets, but included in other recommended diets is DAIRY. This has prompted me to research whether or not dairy has a place in a healthy diet.

The Claim: Dairy is bad for you. You should avoid dairy if you want to have a healthy diet.

Google search: When I searched, “Is dairy bad for you?” I found the following arguments against dairy:

  • Milk is the perfect food, but only for calves
  • Milk doesn’t reduce fractures and may increase your risk of fractures
  • Countries that consume less dairy have the lowest rates of osteoporosis
  • Calcium and/or dairy may increase your risk of prostate cancer
  • 75% of the world’s population is lactose intolerant, especially people that are not of northern European descent
  • If you give up dairy, you should notice improvement with your sinuses, post-nasal drip, headaches, irritable bowel syndrome, energy, and weight
  • Dairy may cause acne

And the following arguments for dairy:

  • Dairy is a good source of nutrition. It includes high amounts of calcium, vitamin D, riboflavin, vitamin B12, potassium and phosphorus. It also contains vitamins A, B1, B6, selenium, zinc and magnesium. Grass-fed, full fat dairy also contains high amounts of omega-3 fatty acids, conjugated linoleic acid and vitamin K2.
  • Dairy improves bone density, reduces osteoporosis, and lowers the risk of fractures
  • Full-fat dairy is associated with a lower risk of obesity, type 2 diabetes, and heart disease
  • Dairy may be protective against colorectal cancer

Follow up questions

  • Are some types of dairy better or worse than others?
  • Is dairy good for some people and bad for others?

Peer-reviewed research

I searched “dairy consumption” on PubMed and included only reviews and meta-analyses. The 26 studies here are the most relevant reviews of how dairy consumption is associated with metabolic syndrome (heart disease, obesity, type 2 diabetes). Several of the studies included cancer and bone health outcomes. However, I did not include studies that only reviewed cancer or bone health outcomes without other components of metabolic syndrome. Of note, I did not come across any reviews that suggested dairy was associated with unfavorable cancer or bone health outcomes.

Complete abstracts are provided below with links to full studies. Many are free to access. Feel free to read them thoroughly, only read the sections in bold, or just skip to the “What We Know and Don’t Know Section”.

  1. Dairy products consumption and metabolic syndrome in adults: systematic review and meta-analysis of observational studies. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26416233
    • The association of dairy products consumption with risk of metabolic syndrome (MetS) has been inconsistently reported in observational studies. A systematic review and meta-analysis of published observational studies was conducted to quantitatively evaluate this association. Relevant studies were identified by searching PubMed and EMBASE databases and by carefully checking the bibliographies of retrieved full reports and related reviews. Eligible studies were observational studies that investigated the association between dairy products consumption and risk of MetS in adults, with risk estimates available. Random-effects model was assigned to calculate the summary risk estimates. The final analysis included 15 cross-sectional studies, one case-control study and seven prospective cohort studies. Higher dairy consumption significantly reduced MetS by 17% in the cross-sectional/case-control studies (odds ratio = 0.83, 95% confidence interval [CI], 0.73-0.94), and by 14% (relative risk [RR] = 0.86, 95% CI, 0.79-0.92) in cohort studies. The inverse dairy-MetS association was consistent in subgroup and sensitivity analyses. The dose-response analysis of the cohort studies conferred a significant 6% (RR = 0.94, 95% CI, 0.90-0.98) reduction in the risk of MetS for each increment in dairy consumption of one serving/d. No significant publication bias was observed. Our findings suggest an inverse dose-response relationship between dairy consumption and risk of MetS.
  2. Yogurt and dairy product consumption to prevent cardiometabolic diseases: epidemiologic and experimental studies. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24695891
    • Dairy products contribute important nutrients to our diet, including energy, calcium, protein, and other micro- and macronutrients. However, dairy products can be high in saturated fats, and dietary guidelines generally recommend reducing the intake of saturated fatty acids (SFAs) to reduce coronary artery disease (CAD). Recent studies question the role of SFAs in cardiovascular disease (CVD) and have found that substitution of SFAs in the diet with omega-6 (n-6) polyunsaturated fatty acids abundant in vegetable oils can, in fact, lead to an increased risk of death from CAD and CVD, unless they are balanced with n-3 polyunsaturated fat. Replacing SFAs with carbohydrates with a high glycemic index is also associated with a higher risk of CAD. Paradoxically, observational studies indicate that the consumption of milk or dairy products is inversely related to incidence of CVD. The consumption of dairy products has been suggested to ameliorate characteristics of the metabolic syndrome, which encompasses a cluster of risk factors including dyslipidemia, insulin resistance, increased blood pressure, and abdominal obesity, which together markedly increase the risk of diabetes and CVD. Dairy products, such as cheese, do not exert the negative effects on blood lipids as predicted solely by the content of saturated fat. Calcium and other bioactive components may modify the effects on LDL cholesterol and triglycerides. Apart from supplying valuable dairy nutrients, yogurt may also exert beneficial probiotic effects. The consumption of yogurt, and other dairy products, in observational studies is associated with a reduced risk of weight gain and obesity as well as of CVD, and these findings are, in part, supported by randomized trials.
  3. The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease. (2013) https://www.ncbi.nlm.nih.gov/pubmed/22810464
    • PURPOSE: To comprehensively review the data on the relationship between the consumption of dairy fat and high-fat dairy foods, obesity, and cardiometabolic disease.
    • METHODS: We have conducted a systematic literature review of observational studies on the relationship between dairy fat and high-fat dairy foods, obesity, and cardiometabolic disease. We have integrated these findings with data from controlled studies showing effects of several minor dairy fatty acids on adiposity and cardiometabolic risk factors, and data on how bovine feeding practices influence the composition of dairy fat.
    • RESULTS: In 11 of 16 studies, high-fat dairy intake was inversely associated with measures of adiposity. Studies examining the relationship between high-fat dairy consumption and metabolic health reported either an inverse or no association. Studies investigating the connection between high-fat dairy intake and diabetes or cardiovascular disease incidence were inconsistent. We discuss factors that may have contributed to the variability between studies, including differences in (1) the potential for residual confounding; (2) the types of high-fat dairy foods consumed; and (3) bovine feeding practices (pasture- vs. grain-based) known to influence the composition of dairy fat.
    • CONCLUSIONS: The observational evidence does not support the hypothesis that dairy fat or high-fat dairy foods contribute to obesity or cardiometabolic risk, and suggests that high-fat dairy consumption within typical dietary patterns is inversely associated with obesity risk. Although not conclusive, these findings may provide a rationale for future research into the bioactive properties of dairy fat and the impact of bovine feeding practices on the health effects of dairy fat.
  4. Dairy products, yogurt consumption, and cardiometabolic risk in children and adolescents. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26175484
    • The high prevalence of obesity in children is a global health issue. Obesity in children and adolescents can result in hypertension, dyslipidemia, chronic inflammation, and hyperinsulinemia, increasing the risk of death, as children grow into adulthood, and raising public health concerns. Type 2 diabetes in children and adolescents is a cardiovascular disease (CVD) risk factor. Dairy consumption may have a protective effect against the development of CVD, but there is scarce evidence of this in children and adolescents. Within the Healthy Lifestyle in Europe by Nutrition in Adolescence, the objective of this study was to investigate the relationship between dairy consumption and CVD risk factors in a sample of adolescents (aged 12.5-17.5 years) from 8 European cities. Overall, dairy products emerged as the food group that best identified adolescents at low CVD risk. Higher consumption of milk and yogurt and of milk- and yogurt-based beverages was associated with lower body fat, lower risk for CVD, and higher cardiorespiratory fitness.
  5. Dairy consumption and pre-school, school-age and adolescent obesity in developed countries: a systematic review and meta-analysis. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24655317
    • Childhood obesity, the primary health problem affecting children in developed countries, has been attributed in part to changes in dietary patterns. Secular trends suggest a decrease in childhood dairy consumption coinciding with the rise in obesity prevalence. The objective of the present systematic review and meta-analysis was to consider evidence of associations between dairy intake and adiposity in pre-schoolers, school-age children and adolescents in developed countries. Of 36 studies included in the systematic review, sufficient data for effect size estimation and inclusion in the meta-analysis were obtained from 22 studies. No significant association was found between dairy intake and adiposity in the aggregated data, although statistical heterogeneity was high (I(2) = 0.72). Among adolescents, however, dairy intake was inversely associated with adiposity (effect size -0.26, [-0.38, -0.14], P < 0.0001). Effect size was not predicted by exposure variable (milk vs. dairy), study design, statistical methods, outcome variables or sex. Interpretation of results was complicated by variability in study methods and insufficient adjustment for relevant confounders, particularly dietary reporting accuracy, sweetened beverage intake and pubertal development. Despite limitations, available data suggest a neutral effect of dairy intake on adiposity during early and middle childhood and a modestly protective effect in adolescence.
  6. Dairy product consumption and the metabolic syndrome. (2015) https://www.ncbi.nlm.nih.gov/pubmed/25605674
    • AIMS: To briefly summarize findings from epidemiological studies on the relationship between dairy product consumption and the metabolic syndrome(MetS).MATERIALS AND METHODS: A search for relevant literature was undertaken on Web of Science, Google scholar, Pubmed (2000 to July 2013), to identify observational studies which examined the association between dairy intake and MetS (prevalence or incidence), and for any randomized controlled trials investigating the effect of dairy intake on MetS.
    • RESULTS: Here we review the physiological effects and possible mechanisms involved of three main dairy constituents (calcium (Ca), protein, fat) on important components of the MetS. Effects of Ca may be related to intestinal binding to fatty acids or bile acids, or to changes in intracellular Ca metabolism by suppressing calciotropic hormones. Dietary proteins may increase satiety in both the short and longer term, which may result in a reduced energy intake. Dairy proteins are precursors of angiotensin-I converting enzyme-inhibitory peptides, which may lower blood pressure. To reduce the intake of saturated fatty acids (SFA), the consumption of low-fat instead of high-fat dairy products is recommended.
    • CONCLUSION: More research is warranted to better understand the physiological effects and the mechanisms involved of dairy products in the prevention and treatment of the MetS.
  7. Dairy products consumption and risk of type 2 diabetes: systematic review and dose-response meta-analysis. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24086304
    • BACKGROUND: The consumption of dairy products may influence the risk of type 2 diabetes mellitus (T2DM), but inconsistent findings have been reported. Moreover, large variation in the types of dairy intake has not yet been fully explored.
    • METHODS AND RESULTS: We conducted a systematic review and meta-analysis to clarify the dose-response association of dairy products intake and T2DM risk. We searched PubMed, EMBASE and Scopus for studies of dairy products intake and T2DM risk published up to the end of October 2012. Random-effects models were used to estimate summary relative risk (RR) statistics. Dose-response relations were evaluated using data from different dairy products in each study. We included 14 articles of cohort studies that reported RR estimates and 95% confidence intervals (95% CIs) of T2DM with dairy products intake. We found an inverse linear association of consumption of total dairy products (13 studies), low-fat dairy products (8 studies), cheese (7 studies) and yogurt (7 studies) and risk of T2DM. The pooled RRs were 0.94 (95% CI 0.91-0.97) and 0.88 (0.84-0.93) for 200 g/day total and low-fat dairy consumption, respectively. The pooled RRs were 0.80 (0.69-0.93) and 0.91 (0.82-1.00) for 30 g/d cheese and 50 g/d yogurt consumption, respectively. We also found a nonlinear association of total and low-fat dairy intake and T2DM risk, and the inverse association appeared to be strongest within 200 g/d intake.
    • CONCLUSION: A modest increase in daily intake of dairy products such as low fat dairy, cheese and yogurt may contribute to the prevention of T2DM, which needs confirmation in randomized controlled trials.
  8. Dairy consumption and CVD: a systematic review and meta-analysis. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26786887
    • Inverse associations between dairy consumption and CVD have been reported in several epidemiological studies. Our objective was to conduct a meta-analysis of prospective cohort studies of dairy intake and CVD. A comprehensive literature search was conducted to identify studies that reported risk estimates for total dairy intake, individual dairy products, low/full-fat dairy intake, Ca from dairy sources and CVD, CHD and stroke. Random-effects meta-analyses were used to generate summary relative risk estimates (SRRE) for high v. low intake and stratified intake dose-response analyses. Additional dose-response analyses were performed. Heterogeneity was examined in sub-group and sensitivity analyses. In total, thirty-one unique cohort studies were identified and included in the meta-analysis. Several statistically significant SRRE below 1.0 were observed, namely for total dairy intake and stroke (SRRE=0·91; 95% CI 0·83, 0·99), cheese intake and CHD (SRRE=0·82; 95% CI 0·72, 0·93) and stroke (SRRE=0·87; 95% CI 0·77, 0·99), and Ca from dairy sources and stroke (SRRE=0·69; 95% CI 0·60, 0·81). However, there was little evidence for inverse dose-response relationships between the dairy variables and CHD and stroke after adjusting for within-study covariance. The results of this meta-analysis of prospective cohort studies have shown that dairy consumption may be associated with reduced risks of CVD, although additional data are needed to more comprehensively examine potential dose-response patterns.
  9. Dairy consumption and risk of metabolic syndrome: a meta-analysis. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26433009
    • AIMS: To conduct a systematic review and meta-analysis of epidemiological studies in order to assess quantitatively the effect of dairy consumption on risk of metabolic syndrome.
    • METHODS: We searched for eligible studies published up to March 2015 through the PubMed and Embase databases and reviewed the references of relevant articles. Random-effects models were used to calculate the pooled relative risks with 95% CIs after adjusting for several confounders.
    • RESULTS: We identified nine prospective cohort studies including a total of 35,379 subjects and 7322 incident cases of metabolic syndrome, and 12 cross-sectional studies including 37 706 subjects. In the meta-analysis of prospective cohort studies, the pooled relative risk of incidence of metabolic syndrome for the highest vs. the lowest category of dairy consumption was 0.85 (95% CI 0.73-0.98), and for a 1-serving/day increment of dairy consumption, the pooled relative risk was 0.88 (95% CI 0.82-0.95). In the meta-analysis of cross-sectional studies, the pooled relative risk of prevalence of metabolic syndrome for the highest vs. the lowest category of dairy consumption was 0.73 (95% CI 0.63-0.86). The association was not significantly different by geographical region, follow-up time and adjustment factors.
    • CONCLUSION: Our findings indicate that dairy consumption is inversely associated with the incidence and prevalence of metabolic syndrome. Further well-designed cohort studies and randomized controlled trials are warranted to provide definitive evidence.
  10. Milk and dairy products: good or bad for human health? An assessment of the totality of scientific evidence. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27882862
    • BACKGROUND: There is scepticism about health effects of dairy products in the public, which is reflected in an increasing intake of plant-based drinks, for example, from soy, rice, almond, or oat.
    • OBJECTIVE: This review aimed to assess the scientific evidence mainly from meta-analyses of observational studies and randomised controlled trials, on dairy intake and risk of obesity, type 2 diabetes, cardiovascular disease, osteoporosis, cancer, and all-cause mortality.
    • RESULTS: The most recent evidence suggested that intake of milk and dairy products was associated with reduced risk of childhood obesity. In adults, intake of dairy products was shown to improve body composition and facilitate weight loss during energy restriction. In addition, intake of milk and dairy products was associated with a neutral or reduced risk of type 2 diabetes and a reduced risk of cardiovascular disease, particularly stroke. Furthermore, the evidence suggested a beneficial effect of milk and dairy intake on bone mineral density but no association with risk of bone fracture. Among cancers, milk and dairy intake was inversely associated with colorectal cancer, bladder cancer, gastric cancer, and breast cancer, and not associated with risk of pancreatic cancer, ovarian cancer, or lung cancer, while the evidence for prostate cancer risk was inconsistent. Finally, consumption of milk and dairy products was not associated with all-cause mortality. Calcium-fortified plant-based drinks have been included as an alternative to dairy products in the nutrition recommendations in several countries. However, nutritionally, cow’s milk and plant-based drinks are completely different foods, and an evidence-based conclusion on the health value of the plant-based drinks requires more studies in humans.
    • CONCLUSION: The totality of available scientific evidence supports that intake of milk and dairy products contribute to meet nutrient recommendations, and may protect against the most prevalent chronic diseases, whereas very few adverse effects have been reported.

  11. Long-term association between dairy consumption and risk of childhood obesity: a systematic review and meta-analysis of prospective cohort studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26862005
    • BACKGROUND/OBJECTIVES: Data from small-scale, short-term, clinical trials suggest a beneficial effect of dairy consumption on the risk of childhood obesity; however, the long-term association is unclear. Therefore, we aim to examine the longitudinal association between dairy consumption and the risk of overweight/obesity in children and adolescents by conducting a systematic review and meta-analysis of prospective cohort studies.
    • SUBJECTS/METHODS: Eligible studies were identified by searching PubMed and EMBASE through March 2015. Additional studies were retrieved via Google Scholar or a hand review of the reference lists from relevant articles. Pooled associations of interest were estimated by using a random-effects model. The heterogeneity for each pooled analysis was evaluated by I(2) statistic as well as by Cochran’s Q test. Publication bias was assessed by using both Egger’s and Begg’s tests.
    • RESULTS: Ten studies comprising 46,011 children and adolescents with an average 3-year follow-up were included. As compared with those who were in the lowest group of dairy consumption, children in the highest intake group were 38% less likely to have childhood overweight/obesity (pooled odds ratio (OR)=0.62; 95% confidence interval (CI): 0.49, 0.80). With each 1 serving/day increment in dairy consumption, the percentage of body fat was reduced by 0.65% (β=0.65; 95% CI: -1.35, 0.06; P=0.07), and the risk of overweight/obesity was 13% lower (OR=0.87; 95% CI: 0.74, 0.98).
    • CONCLUSIONS: Accumulated evidence from prospective cohort studies suggests that dairy consumption is inversely and longitudinally associated with the risk of childhood overweight/obesity. Further studies are warranted to examine the types of dairy products in relation to the risk of childhood overweight/obesity.
  12. Consumption of dairy foods and diabetes incidence: a dose-response meta-analysis of observational studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/26912494
    • BACKGROUND: A growing number of cohort studies suggest a potential role of dairy consumption in type 2 diabetes (T2D) prevention. The strength of this association and the amount of dairy needed is not clear.
    • OBJECTIVE: We performed a meta-analysis to quantify the associations of incident T2D with dairy foods at different levels of intake.
    • DESIGN: A systematic literature search of the PubMed, Scopus, and Embase databases (from inception to 14 April 2015) was supplemented by hand searches of reference lists and correspondence with authors of prior studies. Included were prospective cohort studies that examined the association between dairy and incident T2D in healthy adults. Data were extracted with the use of a predefined protocol, with double data-entry and study quality assessments. Random-effects meta-analyses with summarized dose-response data were performed for total, low-fat, and high-fat dairy, (types of) milk, (types of) fermented dairy, cream, ice cream, and sherbet. Nonlinear associations were investigated, with data modeled with the use of spline knots and visualized via spaghetti plots.
    • RESULTS: The analysis included 22 cohort studies comprised of 579,832 individuals and 43,118 T2D cases. Total dairy was inversely associated with T2D risk (RR: 0.97 per 200-g/d increment; 95% CI: 0.95, 1.00;P= 0.04;I(2)= 66%), with a suggestive but similar linear inverse association noted for low-fat dairy (RR: 0.96 per 200 g/d; 95% CI: 0.92, 1.00;P= 0.072;I(2)= 68%). Nonlinear inverse associations were found for yogurt intake (at 80 g/d, RR: 0.86 compared with 0 g/d; 95% CI: 0.83, 0.90;P< 0.001;I(2)= 73%) and ice cream intake (at ∼10 g/d, RR: 0.81; 95% CI: 0.78, 0.85;P< 0.001;I(2)= 86%), but no added incremental benefits were found at a higher intake. Other dairy types were not associated with T2D risk.
    • CONCLUSION: This dose-response meta-analysis of observational studies suggests a possible role for dairy foods, particularly yogurt, in the prevention of T2D. Results should be considered in the context of the observed heterogeneity.
  13. Systematic Review of the Association between Dairy Product Consumption and Risk of Cardiovascular-Related Clinical Outcomes. (2016) https://www.ncbi.nlm.nih.gov/pubmed/28140321
    • The objective of this systematic review was to determine if dairy product consumption is detrimental, neutral, or beneficial to cardiovascular health and if the recommendation to consume reduced-fat as opposed to regular-fat dairy is evidence-based. A systematic review of meta-analyses of prospective population studies associating dairy consumption with cardiovascular disease (CVD), coronary artery disease (CAD), stroke, hypertension, metabolic syndrome (MetS), and type 2 diabetes (T2D) was conducted on the basis of the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement. Quality of evidence was rated by using the Grading of Recommendations Assessment, Development, and Evaluation scale. High-quality evidence supports favorable associations between total dairy intake and hypertension risk and between low-fat dairy and yogurt intake and the risk of T2D. Moderate-quality evidence suggests favorable associations between intakes of total dairy, low-fat dairy, cheese, and fermented dairy and the risk of stroke; intakes of low-fat dairy and milk and the risk of hypertension; total dairy and milk consumption and the risk of MetS; and total dairy and cheese and the risk of T2D. High- to moderate-quality evidence supports neutral associations between the consumption of total dairy, cheese, and yogurt and CVD risk; the consumption of any form of dairy, except for fermented, and CAD risk; the consumption of regular- and high-fat dairy, milk, and yogurt and stroke risk; the consumption of regular- and high-fat dairy, cheese, yogurt, and fermented dairy and hypertension risk; and the consumption of regular- and high-fat dairy, milk, and fermented dairy and T2D risk. Data from this systematic review indicate that the consumption of various forms of dairy products shows either favorable or neutral associations with cardiovascular-related clinical outcomes. The review also emphasizes that further research is urgently needed to compare the impact of low-fat with regular- and high-fat dairy on cardiovascular-related clinical outcomes in light of current recommendations to consume low-fat dairy.
  14. Dairy products consumption versus type 2 diabetes prevention and treatment; a review of recent findings from human studies. (2013) https://www.ncbi.nlm.nih.gov/pubmed/24160191
    • INTRODUCTION: It has been claimed that the appropriate consumption of dairy products can be beneficial for the prevention and treatment of type 2 diabetes mellitus (T2DM).
    • OBJECTIVE: The objective of this review is to critically analyze the main scientific evidence about this topic.
    • METHODS: MEDLINE, PubMEd, Science Direct, SCIELO and LILACS were searched for studies published over the past 12 years exploring the effects of the consumption of dairy products or its components (calcium, vitamin D and magnesium) on T2DM.
    • RESULTS AND DISCUSSION: Epidemiological studies indicate that consumption of at least three servings of low-fat dairy products per day as a part of a healthy diet is crucial to reduce the risk of developing T2DM. The majority of the analyzed intervention studies reported beneficial effects of increased calcium and vitamin D ingestion on insulin sensitivity improvement and T2DM prevention.
    • CONCLUSIONS: Although the impact of dairy consumption to treat T2DM needs further investigation, the consumption of low-fat dairy products may be an important strategy to prevent and control T2DM.

  15. Meeting and exceeding dairy recommendations: effects of dairy consumption on nutrient intakes and risk of chronic disease. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23550782
    • The 2010 Dietary Guidelines for Americans indicate the US population is experiencing an epidemic of overweight and obesity while maintaining a nutrient-poor, energy-dense diet associated with an increased risk of osteoarthritis, cardiovascular disease, and type 2 diabetes. To build upon the review of published research in the Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010, this article aims to review the scientific literature pertaining to the consumption of dairy foods and the effects of dairy consumption on nutrient intakes and chronic disease risk published between June 2010, when the report was released, and September 2011. PubMed was searched for articles using the following key words: dairy, milk, nutrient intake, bone health, body composition, cardiovascular disease, type 2 diabetes, and blood pressure. Evidence indicates that increasing dairy consumption to the recommended amount, i.e., three servings daily for individuals ≥9 years of age, helps close gaps between current nutrient intakes and recommendations. Consuming more than three servings of dairy per day leads to better nutrient status and improved bone health and is associated with lower blood pressure and reduced risk of cardiovascular disease and type 2 diabetes.
  16. Consumption of Dairy Products in Relation to Changes in Anthropometric Variables in Adult Populations: A Systematic Review and Meta-Analysis of Cohort Studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27310919
    • BACKGROUND: The current state of knowledge regarding the association of dairy products and weight gain, overweight, and obesity is based on studies reporting contradicting and inconclusive results. The aim of the present study was thus to clarify the link between dairy consumption in relation to changes in anthropometric measures/adiposity by a meta-analytical approach.
    • METHODS: For the meta-analysis PubMed, EMBASE, Web of Sciences, and google scholar were searched by two independent authors up to May 2016 with no restriction to language or calendar date. Prospective cohort studies reporting about intake of dairy consumption (including milk, yogurt, cheese, butter) and changes in body weight or waist circumference, risk of overweight, obesity, or weight gain were eligible. Pooled effects were calculated using a random effects model, and also a fixed effect model for sensitivity analysis. Due to the heterogeneity of statistical analytical approaches of the studies the analysis were done separately for beta-coefficients of changes in body weight and/or waist circumference per serving of dairy, for differences in weight gain/gain in waist circumference when comparing extreme categories of dairy consumption, and for odds ratios in regard to weight gain, overweight/obesity, or abdominal obesity.
    • FINDINGS: 24 studies (27 reports) met the inclusion criteria for the systematic review, and 22 studies provided sufficient data for inclusion in the meta-analysis. The meta-analysis of the five studies on changes in body weight per serving of dairy no significant results could be found for whole fat dairy and low fat dairy. However, there was inverse association between changes in body weight for each serving’s increase of yogurt (beta: -40.99 gram/year, 95% CI, -48.09 to -33.88), whereas each serving’s increase of cheese was positively associated (beta: -10.97 gram/year, 95% CI, 2.86 to 19.07). Furthermore, the highest dairy intake category was associated with a reduced risk of abdominal obesity (OR: 0.85; 95% CI, 0.76 to 0.95), and risk of overweight (OR: 0.87; 95% CI, 0.76 to 1.00) compared to the lowest intake category. No significant association could be observed for risk of weight gain.
    • CONCLUSION: In summary the results of the meta-analysis still reflect that dairy consumption was not positively related to changes in body weight. Yogurt was the only dairy food that showed some evidence for a beneficial effect, where higher intakes were inversely associated a reduced risk of obesity, changes in body weight or waist circumference. Further research is needed, since the overall interpretation of the results is limited by heterogeneous risk estimates.
  17. Effect of dairy consumption on weight and body composition in adults: a systematic review and meta-analysis of randomized controlled clinical trials. (2012) https://www.ncbi.nlm.nih.gov/pubmed/22249225
    • BACKGROUND: Although several observational and experimental studies have investigated the effect of dairy consumption on weight and body composition, results are inconsistent.
    • OBJECTIVE: This systematic review and meta-analysis was conducted to summarize the published evidence from randomized controlled clinical trials (RCTs) regarding the effect of dairy consumption on weight, body fat mass, lean mass and waist circumference (WC) in adults.
    • DESIGN: PubMed, ISI Web of Science, SCOPUS, Science Direct and EMBASE were searched from January 1960 to October 2011 for relevant English and non-English publications. Sixteen studies were selected for the systematic review and fourteen studies were included in meta-analysis.
    • RESULTS: Our search led to 14, 12, 6 and 8 eligible RCTs that had data on weight, body fat mass, lean mass and WC, respectively. Overall, mean difference for the effect of dairy on body weight was -0.61 kg (95% confidence interval (CI): -1.29, 0.07, P=0.08). Increased dairy intake resulted in 0.72 kg (95% CI: -1.29, -0.14, P=0.01) greater reduction in fat mass, 0.58 kg (95% CI: 0.18, 0.99, P<0.01) gain in lean mass and 2.19 cm (95% CI: -3.42, -0.96, P-value <0.001) further reduction in WC than that in controls. Subgroup analysis revealed that increasing dairy intake without energy restriction in both intervention and control groups does not significantly affect weight, body fat mass, lean mass and WC; consumption of high-dairy weight loss diets led to 1.29 kg (95% CI: -1.98, -0.6, P<0.001) greater weight loss, 1.11 kg (95% CI: -1.75, -0.47, P=0.001) greater reduction in body fat mass, 0.72 kg (95% CI: 0.12, 1.32, P=0.02) gain in body lean mass and 2.43 cm (95% CI: -3.42, -1.44, P<0.001) additional reduction in WC compared with controls.
    • CONCLUSION: Increased dairy consumption without energy restriction might not lead to a significant change in weight or body composition; whereas inclusion of dairy products in energy-restricted weight loss diets significantly affects weight, body fat mass, lean mass and WC compared with that in the usual weight loss diets.

  18. How sound is the science behind the dietary recommendations for dairy? (2014) https://www.ncbi.nlm.nih.gov/pubmed/24646824
    • This review examined the evidence behind dietary guidelines for dairy. Most countries recommend consumption of dairy products; and when amounts are specified, recommendations are typically for 2 or 3 servings per day. Specific recommendations for dairy products are based partly on culture and availability but primarily on meeting nutrient requirements. Dairy products are a rich source of many minerals and vitamins as well as high-quality protein. Thus, dairy consumption is a marker for diet quality. A recent report found that yogurt specifically is a good marker of diet quality. The food patterns recommended by the 2010 Dietary Guidelines for Americans Advisory Committee (DGAC) include 3 cups of low-fat milk and milk products. Few people achieve their recommended intakes of several shortfall nutrients without meeting their recommendations for dairy. The evidence for a benefit of dairy consumption is moderate for bone health in children but limited in adults and moderate for cardiovascular disease, blood pressure, and diabetes and limited for metabolic syndrome. Newer data since the recommendations of the 2010 DGAC are presented. However, the strength of the evidence for dairy consumption and health is limited by the lack of appropriately powered randomized controlled trials.
  19. Association of dairy products consumption with risk of obesity in children and adults: a meta-analysis of mainly cross-sectional studies. (2016) https://www.ncbi.nlm.nih.gov/pubmed/27756684
    • PURPOSE: The association of dairy products consumption with risk of obesity remains controversial. Therefore, we reviewed and quantitatively synthesized the evidence from observational studies with a meta-analysis.
    • METHODS: A literature search was performed in relevant databases. Random-effects model was used to pool odds ratios with 95% confidence intervals. Dose-response relationship was assessed by restricted cubic spline model.
    • RESULTS: Seventeen studies for total dairy products and 16 studies for milk with risk of obesity were eligible. The pooled odds ratios (95% confidence intervals) of obesity for the highest versus lowest category of total dairy products consumption were 0.54 (0.38-0.77) in children, 0.75 (0.69-0.81) in adults, and 0.74 (0.68-0.80) for both. Evidence of a nonlinear relationship was found (Pfor nonlinearity = .009). Milk consumption was also associated with risk of obesity [0.81 (0.75-0.88)] both in children [0.87 (0.80-0.95)] and in adults [0.77 (0.68-0.87)], and a linear relationship (Pfor nonlinearity = .598) suggested that risk of obesity decreased by 16% [0.84 (0.77-0.92)] for every 200 g/d increment of milk consumption.
    • CONCLUSIONS: This meta-analysis indicates that dairy products consumption may be associated with a decreased risk of obesity. This association may be of public health significance.
  20. Fermented dairy food and CVD risk. (2015) https://www.ncbi.nlm.nih.gov/pubmed/26148916
    • Fermented dairy foods such as yoghurt and cheese are commonly found in the Mediterranean diet. Recent landmark research has confirmed the effect of the Mediterranean diet on reducing the CVD risk, but the relative contributions of fermented dairy foods have not been fully articulated. The present study provides a review of the relationship between fermented dairy foods consumption and CVD risk in the context of the whole diet. Studies show that people who eat healthier diets may be more likely to consume yoghurt, so there is a challenge in attributing separate effects to yoghurt. Analyses from large population studies list yoghurt as the food most negatively associated with the risk of weight gain (a problem that may lead to CVD). There is some suggestion that fermented dairy foods consumption (yoghurt or cheese) may be associated with reduced inflammatory biomarkers associated with the development of CVD. Dietary trials suggest that cheese may not have the same effect on raising LDL-cholesterol levels as butter with the same saturated fat content. The same might be stated for yoghurt. The use of different probiotic cultures and other aspects of study design remain a problem for research. Nevertheless, population studies from a range of countries have shown that a reduced risk of CVD occurs with the consumption of fermented dairy foods. A combination of evidence is necessary, and more research is always valuable, but indications remain that fermented dairy foods such as cheese and yoghurt are integral to diets that are protective against CVD.
  21. Effects of dairy intake on body weight and fat: a meta-analysis of randomized controlled trials. (2012) https://www.ncbi.nlm.nih.gov/pubmed/22932282
    • BACKGROUND: Some intervention studies have suggested that dairy products may influence body weight, but the results remain controversial.
    • OBJECTIVE: We identified and quantified the effects of dairy consumption on body weight and fat mass from randomized controlled trials (RCTs).
    • DESIGN: We conducted a comprehensive search of PubMed and EMBASE databases (to April 2012) of English reports of RCTs regarding dairy consumption on body weight, body fat, or body weight and body fat in adults. The results across studies were pooled by using a random-effects meta-analysis.
    • RESULTS: Twenty-nine RCTs were included with a total of 2101 participants. Overall, consumption of dairy products did not result in a significant reduction in weight (-0.14 kg; 95% CI: -0.66, 0.38 kg; I² = 86.3%). In subgroup analysis, consumption of dairy products reduced body weight in the context of energy restriction or short-term intervention (<1 y) trials but had the opposite effect in ad libitum dietary interventions or long-term trials (≥1 y). Twenty-two RCTs that reported results on body fat showed a modest reduction in the dairy group (-0.45 kg; 95% CI: -0.79, -0.11 kg; I² = 70.9%), and further stratified analysis indicated significant beneficial effects of dairy intervention on body fat in energy-restricted or short-term trials but not in long-term or ad libitum studies.
    • CONCLUSIONS: This meta-analysis does not support the beneficial effect of increasing dairy consumption on body weight and fat loss in long-term studies or studies without energy restriction. However, dairy products may have modest benefits in facilitating weight loss in short-term or energy-restricted RCTs.
  22. Effects of dairy protein and fat on the metabolic syndrome and type 2 diabetes. (2014) https://www.ncbi.nlm.nih.gov/pubmed/25396403
    • The incidence of the metabolic syndrome (MetS) and type 2 diabetes (T2D) is increasing worldwide. Evidence supports a negative relationship between the consumption of dairy products and risk of MetS and T2D. Dairy proteins are known to have a directly beneficial effect on hypertension, dyslipidemia, and hyperglycemia, but a detailed understanding of the underlying mechanisms is missing. It has been confirmed by observations that the insulinotropic effect of dairy proteins is associated with the amino acid composition; in particular branched-chain amino acids (BCAA) seem to be of vital importance. Dairy protein-derived peptides may also contribute to the insulinotropic effect via dipeptidyl peptidase-4 (DPP-4) inhibitory activity, and may lower the blood pressure (BP). The lipid metabolism may be improved by whey protein (WP), which acts to reduce the postprandial triglyceride (TG) response. The effect of dairy fat is much more controversial because of the potentially harmful effect exerted by saturated fatty acid (SFA) on metabolic health. Recent observations suggest less adverse effects of SFA on metabolic health than previous assumed. However, little is known about dairy lipid fractions belonging to the groups of monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), and phospholipids (PL). Dairy fat seems to act differently depending on the dairy product and the composition of macronutrients in the meal. Therefore, for a better understanding of the mechanisms behind the dairy protein and fat effect on MetS, we suggest that more human studies should be carried out to clarify the interactions of dairy protein and fat with macronutrients in the meal and other dairy components, such as micronutrients and microorganisms from fermented products.
  23. Dairy product intake in children and adolescents in developed countries: trends, nutritional contribution, and a review of association with health outcomes. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24330063
    • Despite its contribution to nutrient intake and status, consumption of milk and dairy products by children and adolescents in many countries has waned in recent decades, with a substantial proportion of youth failing to meet intake recommendations. Dairy products remain an important dietary source of multiple micronutrients, including calcium, phosphorus, magnesium, zinc, iodine, potassium, vitamin A, vitamin D, vitamin B12 , and riboflavin (vitamin B2 ). In addition, dairy products provide children with energy, high-quality protein, and essential and nonessential fatty acids. A review of evidence was conducted to evaluate associations between milk or dairy product intake and health outcomes in children and adolescents. Results suggest a neutral or inverse association between consumption of milk and dairy products in children and adolescents and indicators of adiposity, incidence of dental caries, and hypertension. Available data indicate that dairy products are important for linear growth and bone health during childhood. Additional research–in particular, controlled intervention trials and long-term prospective cohort studies–is warranted to better understand how dairy intake affects health outcomes in children and adolescents.
  24. Dairy products on metabolic health: current research and clinical implications. (2014) https://www.ncbi.nlm.nih.gov/pubmed/24445013
    • Dairy products have been thought to have a beneficial role in the metabolic syndrome (MetS). MetS constitutes a cluster of risk factors for an increased mortality, including obesity, impaired glucose homeostasis, hypertension and atherogenic dyslipidemia. Individuals with MetS are also often in a chronic, low-grade inflammatory state. The objective of this review is to examine recent meta-analyses and clinical studies on the association between dairy products consumption and these MetS risk factors. Findings from studies demonstrate that weight loss related to dairy product intake is due to the combination of an energy-restricted diet with consumption of dairy products. Further, a limited number of studies have shown beneficial effects of dairy consumption on plasma lipids, blood pressure, glucose homeostasis or inflammatory and oxidative stress profiles. Overall, this review article suggests that adults should consume at least 2-3 servings of dairy products per day within a well-balanced diet and a healthy lifestyle for metabolic health. Yet, higher dairy product consumption may have additional beneficial effects, but more well-designed intervention studies are needed to ascertain these effects.
  25. Comprehensive Review of the Impact of Dairy Foods and Dairy Fat on Cardiometabolic Risk. (2016) https://www.ncbi.nlm.nih.gov/pubmed/28140322
    • Because regular-fat dairy products are a major source of cholesterol-raising saturated fatty acids (SFAs), current US and Canadian dietary guidelines for cardiovascular health recommend the consumption of low-fat dairy products. Yet, numerous randomized controlled trials (RCTs) have reported rather mixed effects of reduced- and regular-fat dairy consumption on blood lipid concentrations and on many other cardiometabolic disease risk factors, such as blood pressure and inflammation markers. Thus, the focus on low-fat dairy in current dietary guidelines is being challenged, creating confusion within health professional circles and the public. This narrative review provides perspective on the research pertaining to the impact of dairy consumption and dairy fat on traditional and emerging cardiometabolic disease risk factors. This comprehensive assessment of evidence from RCTs suggests that there is no apparent risk of potential harmful effects of dairy consumption, irrespective of the content of dairy fat, on a large array of cardiometabolic variables, including lipid-related risk factors, blood pressure, inflammation, insulin resistance, and vascular function. This suggests that the purported detrimental effects of SFAs on cardiometabolic health may in fact be nullified when they are consumed as part of complex food matrices such as those in cheese and other dairy foods. Thus, the focus on low-fat dairy products in current guidelines apparently is not entirely supported by the existing literature and may need to be revisited on the basis of this evidence. Future studies addressing key research gaps in this area will be extremely informative to better appreciate the impact of dairy food matrices, as well as dairy fat specifically, on cardiometabolic health.
  26. Impact of dairy products on biomarkers of inflammation: a systematic review of randomized controlled nutritional intervention studies in overweight and obese adults. (2013) https://www.ncbi.nlm.nih.gov/pubmed/23446894
    • BACKGROUND: Recent data from cross-sectional studies suggest that consumption of dairy products is inversely associated with low-grade systemic inflammation, but a cause-and-effect relation can be confirmed only with results from randomized controlled trials.
    • OBJECTIVE: We reviewed the results of randomized controlled nutritional intervention studies that have assessed the impact of dairy product consumption (ie, milk, yogurt, and/or cheese) on biomarkers of inflammation in adults (aged ≥18 y).
    • DESIGN: We performed a systematic literature search in PubMed in April 2012, which was limited to randomized controlled trials in humans published in English. Studies that included pregnant or lactating women or that did not include a low-dairy control intervention were excluded.
    • RESULTS: Eight trials that were conducted in overweight or obese adults were included in the review. The only study that had identified change in the inflammatory profile as its primary outcome measure showed that dairy food consumption improved pro- and antiinflammatory biomarker concentrations compared with the low-dairy control diet. Three of the 7 studies in which inflammation was a secondary or undefined outcome showed improvement in key inflammatory biomarkers, ie, C-reactive protein, IL-6, or TNF-α after dairy product consumption, whereas the other 4 studies showed no effect.
    • CONCLUSIONS: Dairy product consumption does not exert adverse effects on biomarkers of inflammation in overweight or obese adults. Several methodologic factors and limitations among existing studies do not allow differentiation between a beneficial or neutral impact of dairy products on inflammation. Further studies specifically designed to assess inflammation-related outcomes are warranted.

What We Know and Don’t Know

  • This topic has been studied extensively. I was able to find more than 20 literature reviews or meta-analyses on how dairy impacts metabolic syndrome. Each of these reviews detailed many other studies of moderate or high quality. In all, tens of thousands of participants of all ages have been studied.

24 of the 26 reviews reported an inverse relationship between dairy consumption and markers of metabolic syndrome. Each study varied in terms of which types of dairy and which markers of metabolic syndrome were studied as well as which findings were the most significant. The two remaining reviews found that increasing dairy in calorie restricted diets helped reduce weight in the short term, but did not help reduce weight in long term non-restricted diets. None of the studies found dairy to be harmful to health in any way. All analyses showed dairy to be either neutral or beneficial to health with a majority claiming benefits for at least one symptom of metabolic syndrome.

Of the studies that separated low-fat from regular-fat dairy, the regular-fat dairy fared either equal to or better than the low-fat. Saturated fat in dairy (including cheese) did not adversely affect participants’ health or blood lipids as expected and several of the reviews called for reconsideration of the recommendation to consume low-fat dairy. A few of the studies continued to recommend low-fat dairy, but this seemed to be due to staying consistent with previous recommendations rather than presenting results showing adverse effects of regular fat dairy.

Of the studies that separated different dairy products, yogurt consistently had the most favorable outcomes. Yogurt seemed especially protective against cardiovascular disease, obesity, and type 2 diabetes. One study found that people who consumed more cheese were more likely to be obese, but this finding was not consistent across the research.

A few of the studies focused on children and adolescents. They found that the children who consumed the most dairy had the fewest problems with obesity.

Most of the studies found an inverse relationship between dairy consumption and markers of metabolic syndrome. That suggests that the more dairy a person consumes, the healthier they are. Some studies recommended 2-3 servings per day while other recommended more than 3.

The research I found did not address the topic of lactose intolerance. The majority of the research I found was done on participants from “developed” countries that recommended dairy in their health guidelines. These included the U.S., Canada, and Europe. Therefore, it’s hard to say whether the outcomes would apply to Africa and Asia. Common sense would suggest that people who are lactose intolerant should avoid dairy or use medication to assist digestion.

Conclusions and Applications

If you’re not lactose intolerant, you can and should include dairy in your healthy diet. Regular-fat is just as good, or, maybe even better for you than low-fat. Consuming about 3 servings of dairy per day, especially yogurt and milk, is likely to be beneficial to your health. The benefits include helping you maintain a healthy weight, decreasing your likelihood of developing heart disease and type 2 diabetes, and providing tons of necessary nutrients. Although I did not specifically research the association between dairy and cancer or bone health, the evidence I came across all suggests dairy is beneficial in these areas as well.

Dairy is not as it seems, likely to be the reason people who follow a paleo or vegan diet tend to be healthier. Perhaps simply cutting large groups of food out of your diet tends to make you eat less overall. Or maybe it makes you more likely to cook healthy foods at home rather than go out and risk being unsure of which ingredients are being used.

Based on a TON of research, we can confidently keep dairy in the “healthy” category. Evidence supports all the traditional paleo foods, all the plant-based vegan foods, and all the dairy as good for health. The general consensus across all nutrition camps still discourages consumption of highly processed foods, refined grains, and added sugar. The jury is still out on saturated fat, so that will be my next topic to tackle!

Is Advil Preventing You From Getting Pregnant?

This month, I’m taking a break from diet to explore another important area in health and wellness: fertility. Any girl who’s ever turned to Google or Pinterest in search of increasing fertility has no doubt encountered hundreds of tips and tricks. As usual, some are reliable and others are based on myth and anecdote.

Eat vegan. Eat Paleo. Eat whole-30. No smoking. No alcohol. Some alcohol. No caffeine. Some caffeine. Prenatal vitamins. Ovulation predictors. Work out more. Work out less. Yoga. Acupuncture. Hypnosis. Basal body temperature. Do it every day. Don’t do it every day. Test for STDs. Get a semen analysis. Test your tubes. Test for endometriosis.

One recommendation in particular caught my attention. I came across a headline saying that NSAIDs (non-steroidal anti-inflammatory drugs) can prevent ovulation. I had never heard about this before and decided to take a deeper look.

NSAIDs are over-the-counter pain medications that work by blocking enzymes that make prostaglandins (which cause swelling and are interpreted as pain). Many people take these medications fairly often for headaches, backaches, joint pain, menstrual cramps, toothaches, other injuries, and even heart disease.

Some common OTC NSAIDs are: Aspirin (Bayer, Excedrin), Ibuprofen (Advil, Motrin, Nuprin), Ketoprofen (Actron, Orudis), and Naproxen (Aleve). Others are available with a prescription.

The Claim: Taking NSAIDs can reduce fertility by preventing ovulation.

Initial Search: A quick Google search came up with the following results:

WebMD: NSAIDs may hinder ovulation and lower levels of the female hormone progesterone. They cite a study by Sami Salman, MD, from the University of Baghdad. This study is available below in the peer-reviewed research section. Essentially, he studied 39 women taking either an NSAID or a placebo for 10 consecutive days, beginning on day 10 of the menstrual cycle. Ovulation was reduced by 75-93% depending on which drug the patients were taking compared to the control group. He stated that progesterone levels also dropped for the experimental groups. After discontinuing treatment, all of the women ovulated normally during their next cycle. Dr. Salman even proposed that these findings could help them develop a new contraceptive.

Medscape: Pharmacist Darrell Hullsz describes how some side effects of NSAIDs are well known including gastrointestinal, cardiovascular, and renal problems as well as problems toward the end of pregnancy. He says that problems with ovulation have been reported for several decades, but that these problems are still not widely known. An enzyme, COX-2, that is active in the ovaries during follicular development, is blocked by NSAIDs. This prevents the follicule from rupturing (egg from being released). Women see all the other signs of ovulation including elevated body temperature and progesterone levels, but the egg is never released. He goes a step further stating that COX-2 inhibitors may also disrupt fertilization, implantation, and establishment of the placenta. He references the study mentioned above by WebMD as well as two other studies listed below in the peer-reviewed section that oppose the claim by suggesting that delayed follicular rupture is unlikely to cause infertility.

Many other popular health news websites also cite Dr. Salman’s study including: ScienceDaily, Daily Mail, Pharmaceutical Journal, Holistic Primary Care, TheraSpecs, and many fertility blogs and centers.

Follow-up Questions:

If NSAIDs really do affect fertility, does timing and dosage matter? Would it be ok to take NSAIDs during your period, but avoid it during the middle and end of your cycle? Is a lower dose safer?

Are there other painkillers that are safer to take when trying to conceive?

Peer reviewed Research:

These are all of the relevant studies I found. Most did not have full text available. I have provided abstracts with the most important findings from each study in bold.



Background: NSAIDs are popular and used as analgesics, antipyretics and anti-inflammatory agents for more than a century. They are sold without a prescription and taken by millions of patients every day all over the world. There has been recent concerns as to their use in females at child bearing age, as many animal studies showed unfavourable effects on ovulation.

Objectives: To study the effects of short term use of NSADs at their conventional dosages on ovulation.

Methods: Thirty nine women at fertile age were chosen as volunteers to take part in this study, they visited the Rheumatology consultation clinic in Baghdad Hospital, suffering from minor backpain and received one of the three test drugs (diclofenac 100mg once daily, naproxen 500mg twice daily & etoricoxib 90mg once daily). Treatment with the above drugs was given for ten days starting at day ten of the onset of the menstrual cycle. A blood sample was taken from each patients for hormonal analysis (progesterone level) together with an ultra sonsography to assess the mean diameter of the dominant follicle. At day twenty the patient came back for another ultra sonography & to give a blood sample for another check for progesterone level. A fourth group served as controls, who received no treatment (control volunteers).

Results: There was significant inhibition of ovulation in patients treated with diclofenac, naproxen & etoricoxib. Diclofenac was the highest inhibitor of ovulation compared to the other two drugs (naproxen & etoricoxib). A significant decrease in progesterone level in all three groups in compared to the control group was found. Functional cysts have been observed in one third of patients by the end of the treatment period with diclofenac, naproxen & etoricoxib due to unruptured follicles these disappeared at the next cycle.

Conclusions: The findings may serve as an alarm of the harmful effects of these drugs on female fertility and be taken into consideration in females planning to have a child. The above results may open the door for looking for an emergency contraceptive safer than those at use.



Ovulation constitutes the central event in ovarian physiology, and ovulatory disfunction is a relevant cause of female infertility. Non-steroidal anti-inflammatory drugs (NSAIDs), widely used due to their analgesic and anti-inflammatory properties, consistently inhibit ovulation in all mammalian species investigated so far, likely due to the inhibition of cyclooxygenase 2 (COX-2), the inducible isoform of COX, that is the rate-limiting enzyme in prostaglandin (PG) synthesis. COX-2 inhibition has major effects on ovulation, fertilization and implantation, and NSAID therapy is likely implicated in human infertility and could be an important, frequently overlooked, cause of ovulatory disfunction in women. Although there is compelling evidence for a role of PGs in ovulation, the molecular targets and the precise role of these compounds in the ovulatory process are not fully understood. Morphological studies from rats treated with indomethacin (INDO), a potent inhibitor of PG synthesis, provide evidence on the actions of NSAIDs in ovulation, as well as on the possible roles of PGs in the ovulatory process. Cycling rats treated with INDO during the preovulatory period show abnormal ovulation, due to disruption of the spatial targeting of follicle rupture at the apex. Noticeably, gonadotropin-primed immature rats (widely used as a model for the study of ovulation) show age-dependent ovulatory defects similar to those of cycling rats treated with INDO. These data suggest that NSAID treatment disrupts physiological mechanisms underlying spatial targeting of follicle rupture at the apex, which are not fully established in very young rats. We summarize herein the ovulatory defects after pharmacologic COX-2 inhibition, and discuss the possible mechanisms underlying the anti-ovulatory actions of NSAIDs.



Nonsteroidal anti-inflammatory drugs (NSAIDs) are frequently prescribed to women of child-bearing age. Three case series highlight the possibility of a link between NSAIDs and reversible infertility. The pharmacological target of NSAIDs is cyclo-oxygenase (COX), which catalyses the first rate-limiting step in the production of prostaglandins. COX-2, one of two isoenzymes, is active in the ovaries during follicular development. Its inhibition is thought to cause luteinised unruptured follicle (LUF) syndrome, an anovulatory condition characterised by clinical signs of ovulation but in the absence of follicular rupture and ovum release. The evidence linking regular NSAID use to reversible LUF syndrome comes from animal studies and three clinical studies. COX-2-deficient mice have severely compromised ovulation in the presence of apparently normal follicular development. Experimental administration of prostaglandins induced ovulation in rabbits and this was blocked by the administration of indomethacin. The three clinical studies demonstrated the induction of delayed follicular rupture or LUF in previously ovulating women by the administration of NSAIDs. A link can therefore be identified between NSAID use and reversible female infertility and NSAID withdrawal should be considered prior to or concurrent with fertility investigations.



BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) and selective cyclooxygenase-2 inhibitors may interfere with ovulation and the rupture of the follicle, causing reversible infertility.

METHOD: Literature review.

RESULTS: Reversible infertility is shown both in animal and human studies of these drugs. As determined by ultrasound, the drugs may delay or inhibit ovulation. These findings are also confirmed by a few randomized controlled studies showing an increase in time from the luteinizing hormone surge to rupture of the follicle and an increased size of the unruptured follicle. Most of the hormone analyses show values in accordance with the ovulation/menstrual cycle. Also, two epidemiological studies have shown an association between NSAID use and spontaneous abortion. These studies have methodological weaknesses and their findings have to be elucidated in future studies.

INTERPRETATION: Women with fertility problems should avoid not only the selective cyclooxygenase-2 inhibitors, but also the traditional NSAIDs. However, women with rheumatic disease responding well to therapy should consult their physicians before stopping treatment. Reduced dose of a NSAID and temporary stop of drug treatment early in the menstrual cycle, or alternative drug treatment, may be a solution. NSAIDs should not be used in the last eight weeks of pregnancy.

  • 5. Reversible ovulatory failure associated with the development of luteinized unruptured follicles in women with inflammatory arthritis taking non-steroidal anti-inflammatory drugs. (1996) https://www.ncbi.nlm.nih.gov/pubmed/8646437



The case histories of three young women with ankylosing spondylitis, rheumatoid arthritis and a seronegative inflammatory polyarthritis undergoing investigations for infertility are presented. In each, non-steroidal anti-inflammatory drug (NSAID) therapy was associated with the recurrent development of luteinized unruptured ovarian follicles and normal ovulation following drug withdrawal. It is suggested that NSAID therapy may be an important and frequently overlooked cause of anovulation and infertility.


Abstract (1) There have been isolated reports of reversible female infertility linked to NSAIDs. The likely mechanism is ovulatory failure due to non rupture of mature follicles. (2) If a woman who presents with infertility is found to be taking a NSAID, the role of the drug should be considered before launching costly, invasive investigations or starting medically assisted reproduction.



OBJECTIVE: To highlight the possible association between infertility and treatment with long-term non-steroidal anti-inflammatory drug (NSAIDs). NSAIDs act mainly through the inhibition of cyclooxygenase, the enzyme that catalyses the synthesis of prostaglandins, which are essential mediators of ovulation, implantation and placentation of the conceptus.

METHODS: Case reports of four women suffering from severe arthritis, on long-term NSAIDs and undergoing extensive investigation and treatment for infertility.

RESULTS: During the last 2 yr, four out of five women with severe arthritis and difficulty conceiving were counselled to stop NSAIDs, and they successfully conceived shortly after the withdrawal of NSAIDs.

CONCLUSION: NSAIDs, used largely for the treatment of rheumatological conditions, may be responsible for some cases of infertility.


Abstract: Non-steroidal anti-inflammatory drugs are widely used in the treatment of inflammatory joint diseases. Many patients suffering from these disorders are young women during their childbearing years. We report three cases of infertility where the cause may have been NSAID-induced ‘luteinized unruptured follicle’ syndrome. This phenomenon is well recognized in obstetric circles, and we would like to bring it to the attention of rheumatologists since it is not documented in the rheumatological literature.



STUDY QUESTION: Does use of commonly used over-the-counter (OTC) pain medication affect reproductive hormones and ovulatory function in premenopausal women?

SUMMARY ANSWER: Few associations were found between analgesic medication use and reproductive hormones, but use during the follicular phase was associated with decreased odds of sporadic anovulation after adjusting for potential confounders.

WHAT IS KNOWN ALREADY: Analgesic medications are the most commonly used OTC drugs among women, but their potential effects on reproductive function are unclear.

STUDY DESIGN, SIZE, DURATION: The BioCycle Study was a prospective, observational cohort study (2005-2007) which followed 259 women for one (n = 9) or two (n = 250) menstrual cycles.

PARTICIPANTS, SETTING, METHODS: Two hundred and fifty-nine healthy, premenopausal women not using hormonal contraception and living in western New York state. Study visits took place at the University at Buffalo.

MAIN RESULTS AND THE ROLE OF CHANCE: During study participation, 68% (n = 175) of women indicated OTC analgesic use. Among users, 45% used ibuprofen, 33% acetaminophen, 10% aspirin and 10% naproxen. Analgesic use during the follicular phase was associated with decreased odds of sporadic anovulation after adjusting for age, race, body mass index, perceived stress level and alcohol consumption (OR 0.36 [0.17, 0.75]). Results remained unchanged after controlling for potential confounding by indication by adjusting for ‘healthy’ cycle indicators such as amount of blood loss and menstrual pain during the preceding menstruation. Moreover, luteal progesterone was higher (% difference = 14.0, -1.6-32.1, P = 0.08 adjusted) in cycles with follicular phase analgesic use, but no associations were observed with estradiol, LH or FSH.

LIMITATIONS, REASONS FOR CAUTION: Self-report daily diaries are not validated measures of medication usage, which could lead to some classification error of medication use. We were also limited in our evaluation of aspirin and naproxen which were used by few women.

WIDER IMPLICATIONS OF THE FINDINGS: The observed associations between follicular phase analgesic use and higher progesterone and a lower probability of sporadic anovulation indicate that OTC pain medication use is likely not harmful to reproduction function, and certain medications possibly improve ovulatory function.



OBJECTIVE: To assess the effect of ibuprofen, a nonspecific inhibitor of prostaglandin synthesis, on ovulation.

DESIGN: Prospective, randomized, double-blind, placebo-controlled cross-over study.

SETTING: University Medical Center.

PATIENT(S): Twelve normally cycling women between ages 20 and 40.

INTERVENTION(S): Subjects were randomized to either oral ibuprofen (800 mg) or placebo three times per day, beginning when the maximum diameter of the leading follicle reached 16 mm by ultrasound, and continuing for 10 days total. The second cycle was a washout period, and in the third cycle, the subjects were crossed over to the alternate regimen from the first cycle. The probability of delayed follicular collapse was determined using the binomial distribution, and changes in P levels were compared using the paired t test.

MAIN OUTCOME MEASURE(S): Urinary LH surge, follicular collapse by serial transvaginal ultrasonography, and serum midluteal P levels.

RESULT(S): Eleven of 12 subjects detected an LH surge with both ibuprofen and placebo. Five of 11 women demonstrated a >or=2-day increase in time interval from detection of the LH surge to follicular collapse, and 3 of those 5 had been randomized to ibuprofen. This represents a 27% (3 of 11; 95% confidence limits: 1%, 53%) rate of delay for follicular collapse for ibuprofen. There was no difference in average midluteal P levels for ibuprofen or placebo.

CONCLUSION(S): If ibuprofen inhibits follicular collapse, this effect is seen in a small group of study subjects, and this information should be clinically reassuring to patients who take nonsteroidal anti-inflammatory drugs. Serum midluteal P levels were unaffected by administration of ibuprofen.

What we know and don’t know

The research I found doesn’t give us a very definitive answer. 8 out of the 10 studies or reviews point to a strong association between NSAIDs and ovulation problems. However, in most of these studies, subjects took high doses for an extended period of time (at least 10 consecutive days). Some of them used NSAIDs that are unpopular or unavailable in the US. 1 out of the 10 studies suggests a weak association between NSAIDs and ovulation problems and 1 out of the 10 studies actually suggests that NSAIDs can improve ovulation.

Here is a table to help make the findings more clear

Study number Number/description of subjects Type of study Outcome with NSAIDs
1 39 women Control trial (non-random) poor
2 rats Unsure, review? poor
3 3 women Case studies poor
4 unsure Review poor
5 3 women Case studies poor
6 “isolated reports” Review poor
7 4 women Case studies poor
8 3 women Case studies poor
9 259 women Control trial (non-random) good
10 12 women Randomized control trial Poor in a small group


The majority of studies reporting poor outcomes are case studies involving 3 or 4 women. They may even be citing the same 3 or 4 women in multiple articles. It is difficult to know details (such as exactly which medications the women were taking and for how long) from the abstracts. However, we do know that in study 1 most of the women were taking medications not available in the US. In study 9 however, the women were mostly using Advil. This might make findings from study 9 more relevant. Study 10 is the highest quality in terms of research design, but with only 12 subjects, the results may not be reliable.

The possible mechanism responsible for ovulation problems while using NSAIDs is well described and seems plausible. According to this research, it has been observed in all mammals. However, studies involving mice and rats may still not be relevant to humans.


Overall, it seems like there is some good evidence to suggest that taking NSAIDs regularly can cause problems with ovulation. Unfortunately, there is still some controversy. I wasn’t able to find any good information on lower doses or the importance of timing, but subjects in these studies all took the medications around the time of ovulation.

I was also unable to find any information on good alternatives. Study 9, which claimed painkillers do not cause ovulation problems, didn’t separate out NSAIDs and acetaminophen. A quick Google search suggests that acetaminophen (like Tylenol) is safe during pregnancy, but may reduce estrogen and luteinizing hormones in the body. This could affect fertility.  I have yet to look deeper into this claim.


My recommendation would be for anyone who has had unexplained infertility for more than 3 months to stop taking NSAIDs and use Tylenol for mild/occasional pain relief (unless your doctor doesn’t think this would be safe). Fertility treatments are often very expensive and might be avoided by simply switching pain medication.