Can Grilled Foods Cause Cancer?



Grilling your food over an open flame can cause cancer.

Initial search

Many different foods have been blamed for causing cancer over the years. Some people accuse red meat or processed meat. Others are sure sugar is to blame. Still others cite animal studies that conclude genetically modified foods are the culprit.

I’ve read several sources that say what we eat actually matters LESS than how we cook it. A quick internet search turned up many sources that claim cooking foods, especially meat, over an open flame could be the most concerning of all.

According to, heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs) are what we need to watch out for. HCAs are formed when meats are cooked at high temperatures while PAHs are formed when foods are exposed to smoke.

Well-done, grilled, pan-fried or barbecued meats that are cooked at temperatures above 300 degrees are likely to have more HCAs than meats that are baked, cooked slowly over low heat, or are less well-done.

When foods containing HCAs or PAHs are eaten, enzymes in the body start to break them down and make them capable of damaging DNA. This process is called bioactivaiton. Enzymes involved in bioactivation may vary among different people. sites animal studies that suggest HCAs and PAHs cause various types of cancers in rodents when fed in large amounts (thousands of times the amounts humans would typically consume). Associations have also been found between certain cancers and frequent consumption of meats cooked at high temperatures in large epidemiologic studies.

The World Cancer Research Fund and the American Institute for Cancer Research issued dietary guidelines recommending limited consumption of red, processed, and smoked meats. However, no recommendations were provided for HCA and PAH levels. mimics these concerns. The site states that human studies haven’t been able to find strong cancer associations like the animal studies, but you might still want to err on the side of caution. The authors recommend removing burned or charred portions of meats because HCAs are only found there. Additionally, since smoke is often formed by fat dripping from the meat, they recommend using low-fat meats. Finally, they suggest that marinating meat helps lessen HCA formation due to antioxidants in herbs and spices.

A similar article in Men’s Health Magazine recommends putting foil over the grill to avoid too much smoke and eating lots of veggies to increase your antioxidants. Other articles, including one by the Washington Post, have similar advice. They state that grilling (even burning) vegetables does not pose the same risk as grilling meats.

Unlike most of the topics I research, there isn’t much debate over this one. The consensus is that meats cooked at high heats or over an open flame may cause cancer if you eat them often. However, I didn’t find any articles exaggerating the evidence. Instead, they suggest limiting these meats to around once a week and using simple strategies to decrease the risks. I’m still curious to see what the research says. Just how dangerous are these meats?

Peer reviewed research (Or click here
to skip to the discussion)

  1. A review and meta-analysis of prospective studies of red and processed meat, meat cooking methods, heme iron, heterocyclic amines and prostate cancer. (2015)

This meta-analysis reviewed 19 different cohort studies and DID NOT reveal significant patterns of associations between red or processed meat and prostate cancer. Cooking methods were addressed in 5 of the 19 studies and again there was NO association between high temperature cooking and prostate cancer.

2. Are meat and heme iron intake associated with pancreatic cancer? Results from the NIH-AARP Diet and Health Cohort (2016)

This cohort study reviewed dietary patterns of 322,846 participants over 10 years. They found significant associations between pancreatic cancer in men and red meat, meat cooked at high-temperature, grilled/barbequed meat, well/very well done meat, and heme iron from red meat. Surprisingly, they only found a significant association between pancreatic cancer in women and intake of white meat.

3. A prospective study of meat, cooking methods, meat mutagens, heme iron, and lung cancer risks. (2009)

This study reviewed dietary patterns and cooking methods in 278,380 men and 189,596 women. There was a moderate association between red meat consumption and lung cancer. They proposed this might be explained by heme iron intake and high-temperature cooking.

4. Grilled, Barbecued, and Smoked Meat Intake and Survival Following Breast Cancer. (2017)

This study followed 1508 women who were diagnosed with breast cancer in 1996 and 1997. 5 years later, 597 of the women had died, 237 from breast cancer related causes. Researchers found that women with continued high grilled/barbecued and smoked meat intake after diagnosis were 31% more likely to die of any cause. They also found that breast-cancer specific mortality was decreased among women with any pre- and post diagnosis intake of smoked poultry of fish. This suggests that all meats may not affect us equally. Smoked poultry or fish may be less harmful than other meats.

5. Meat intake, cooking methods, dietary carcinogens, and colorectal cancer risk: findings from the Colorectal Cancer Family Registry. (2015)

This study reviewed diets and cooking methods for 3364 cases of colorectal cancer as well as several thousand unaffected family members and controls. The main finding was a positive association between pan-fired beef steak and colorectal cancer. The also found borderline significant associations with colorectal cancer for diets high in oven-broiled ribs. Surprisingly, they found an inverse association between colorectal cancer and grilled hamburgers and no association with total non-processed red meat or total processed meat. The authors noted that the associations were more prominent with a certain gene expression (MMR deficiency)

6. Meat-related compounds and colorectal cancer risk by anatomical subsite. (2013)

This study compared the diets of 989 people with colorectal cancer and 1033 controls. Positive associations were found with processed meat and pan-fried red meat. However, inverse associations were found with poultry, even when grilled, well-done or charred. The authors noted that this was unexpected.

7. Grilled meat consumption and PhIP-DNA adducts in prostate carcinogenesis. (2001)

This study concluded that reduction of grilled red meat (but not white meat) consumption may reduce prostate cancer risk.

8. How do you want your steak prepared? The impact of meat consumption and preparation on prostate cancer. (2012)

This study analyzed the diets of 982 men with prostate cancer. They found associations with ground beef, processed meat, and well done meat. There was no association with rare or less cooked meat. The study only addressed red meat.

9. Impact of meat consumption, preparation, and mutagens on aggressive prostate cancer. (2011)

This study included 470 cases of prostate cancer and 512 controls. Higher consumption of well-done ground beef or processed meats were associated with aggressive prostate cancer. In contrast, consumption of rare/medium cooked ground beef was not associated with aggressive prostate cancer.

10. Dietary Intake of Meat Cooking-Related Mutagens (HCAs) and Risk of Colorectal Adenoma and Cancer: A Systematic Review and Meta-Analysis. (2017)

This meta-analysis reviewed 39 studies and concluded that “mutagenic compounds” (HCAs) formed during cooking of meat at high temperatures may be responsible for colorectal cancer.

11. Red meat-derived heterocyclic amines increase risk of colon cancer: a population-based case-control study. (2013)

This study interviewed 1062 people with colon cancer and 1645 controls. They concluded that HCAs and PAHs from well-done red meat, but not white meat, was associated with colon cancer.

12. Dietary heterocyclic amines and cancer of the colon, rectum, bladder, and kidney: a population-based study. (1999)

This study looked at diets of 553 controls, 352 cases of colon cancer, 249 cases of rectal cancer, 273 cases of bladder cancer, and 138 cases of kidney cancer. Researchers estimated average daily intake of HCAs to be 60-100 nanograms. Only intakes of above 1900 nanograms were associated with cancer. (7 of the cancer patients had intakes this high whereas none of the controls did.

What We Know and Don’t Know

Ok, so what does all this mean? Most of these articles seem to support the hypothesis that well-cooked meat causes cancer. On the surface, that appears to be true. But, after looking at all this data, I’m not convinced it’s something we should worry too much about.

Why? Well, for starters, most of the studies only found associations with red meat. With the exception of a weak association in one study, white meat and fish are off the hook. (pun).

Second, these are epidemiological and/or prospective cohort studies, NOT trusty randomized controlled trials. To review, a prospective cohort study follows a group of similar individuals over a long period of time to see what will happen with regards to a certain outcome (like cancer). Epidemiological studies look at large populations and try to find associations.

It is clear that certain cancers, especially colorectal and prostate cancers, are associated with high intakes of well-done red meat. However, it is possible that other factors that were not controlled for could be at play. Also, there were plenty of people in all of these studies that ate lower amounts of well-done meats and still got cancer. The associations reported were significant, but weak. There are probably other factors (like genetics) that more strongly contribute to your chances of getting cancer.

Conclusions and applications

Because well-controlled animal studies also show that red meats cooked at high temperatures may cause cancer, I wouldn’t completely disregard the weaker evidence from human studies.

However, I wouldn’t go out of my way to change my eating habits unless I was eating well-done red meat nearly every day. You would be better off paying attention to things like sugar intake and overall calories before worrying about how you should or shouldn’t cook your meat.

If I was in the habit of eating well-done burgers most days, I’d cycle them out with chicken or fish to minimize cancer risks and stay healthier overall.

Should I take a Probiotic?

probiotics 2

The Claim

You should take probiotic pills or eat probiotic foods for a healthy gut.

Initial search

What exactly are probiotics? According to WebMD, probiotics are live bacteria and yeasts that are good for you and your digestive system. Everyone has bacteria in their lower digestive tract. In fact, there are more bacteria in your intestines than cells in your body! Everyone has both “good” and “bad” bacteria. In healthy people, the good bacteria are able to keep the bad bacteria in check. However, sometimes the good bacteria can be killed off, allowing the bad bacteria to take over and cause problems ranging from diarrhea and constipation to weight gain and skin conditions.

In order to help people maintain an optimal bacteria balance, some doctors recommend supplementing with probiotics, or “good” bacteria. Probiotics are available in pill form, and can also be found in fermented foods such as certain dairy products, sauerkraut, kimchi, and kombucha.

There are many types of probiotics and products available. Some claim to contain more than 100 billion live bacteria (called colony-forming units or CFUs) in each pill while others claim numbers in the millions. Some need to be refrigerated and others don’t. Some might get destroyed by stomach acid while others might not. Some were made in labs and have detailed information about genus, species, and strain while others were made in your neighborhood hippie’s backyard.

The science around gut bacteria has really gotten underway in the past decade, but there is still a lot of gray area and a lot we don’t know. This has made probiotic supplementation a controversial topic. Should everyone take a probiotic? How much do we need? Which strains? Which conditions can they help and how? Some researchers think they have answers to these questions while others are more hesitant.

Some claims made by those who support probiotic supplementation include:

  • They help with weight management
  • They treat and prevent diarrhea and constipation as well as other gut disorder such as Crohn’s disease, IBS, ulcerative colitis, and necrotizing enterocolitis
  • They can improve mental health conditions including: anxiety, depression, autism, obsessive-compulsive disorder, and memory via the gut-brain connection
  • They can help regulate insulin, and reduce inflammation, blood pressure and LDL
  • They can reduce symptoms of allergies and eczema
  • They improve sperm motility
  • Decrease tooth decay and gum disease
  • They can “boost your immune system” to decrease your chances of getting respiratory infections and urinary tract infections
  • They help prevent cancer

What the skeptics say:

  • The current research only supports treatment for certain types of diarrhea (such as that caused by antibiotics). And scientists still aren’t exactly sure how that works.
  • We don’t really know how much you need or which strains work best for which diseases.
  • We don’t really know why they seem to work for some people and not others.
  • They might actually cause problems for people with weak immune systems.
  • Probiotics have been shown NOT to change the composition of bacteria in fecal matter in healthy people
  • Enthusiasm for probiotics has outpaced the scientific evidence.
  • Until we know more, probiotics are a waste of money.

Peer reviewed research

Or click here to skip the research.

First, I conducted a search of meta-analyses of RCTs. These were all done in the past 5 years using human participants.

1. Probiotics for Gastrointestinal Conditions: A Summary of the Evidence. (2017)

This summary of the evidence states that certain probiotics are effective for: acute infectious diarrhea, antibiotic-associated diarrhea, Clostridium difficile- associated diarrhea, hepatic encephalopathy, ulcerative colitis, irritable bowel syndrome, functional gastrointestinal disorders, and necrotizing enterocolitis. It states they are not effective for: acute pancreatitis and Crohn disease.

2. The role of probiotics in prevention of oral diseases. (2016)

This review concluded that certain probiotics can help prevent cavities, gum disease, and bad breath.

3. Probiotics in dermatologic practice. (2016)

This review looked at all the data surrounding probiotic use for skin conditions. They found enough evidence to recommend probiotic treatment for atopic dermatitis. They mentioned other conditions which needed further research.

4. Probiotics-mediated suppression of cancer. (2017)

Researchers concluded that the data for using probiotics in cancer treatment is encouraging, but insufficient to recommend their use as an alternative therapy.

5. Clinical Uses of Probiotics. (2016)

This review concluded that the data supports probiotic use for GI-related illnesses, but not for most other conditions. The article goes into depth regarding probiotic strains and compositions.

6. Probiotics for managing caries and periodontitis: Systematic review and meta-analysis. (2016)

This review concluded that probiotics may help reduce or prevent gum disease, but the evidence for preventing and treating cavities is insufficient.

7. Systematic review: probiotics for functional constipation in children. (2017)

This review found that probiotics had little on constipation in children.

8. Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. (2017)

This review of the evidence supports probiotic treatment for people at risk for C-diff associated diarrhea.

9. Effectiveness of probiotics in irritable bowel syndrome: Updated systematic review with meta-analysis. (2015)

This review found that probiotics reduce pain and severity of symptoms in many people with IBS.

10. Probiotics for weight loss: a systematic review and meta-analysis. (2015)

This review found that RCTs generally do not support the use of probiotics to assist in weight loss. No significant differences were found in treatment versus control groups.

11. Probiotics and Subclinical Psychological Symptoms in Healthy Participants: A Systematic Review and Meta-Analysis. (2017)

This review included 7 randomized placebo controlled clinical trial which tested whether probiotics could improve depression, anxiety, and stress. They concluded that probiotics significantly improved psychological symptoms in healthy adults.

12. Effect of Probiotics on Depression: A Systematic Review and Meta-Analysis of Randomized Controlled Trials. (2016)

This review included 12 RCTs and found that probiotics significantly reduced symptoms of depression in people under age 60, but not in older adults.

13. Efficacy of probiotics on anxiety-A meta-analysis of randomized controlled trials. (2018)

This meta-analysis included 12 RCTs which, together, showed no significant difference between treatment and placebo groups.

Next, I conducted a search on randomized controlled clinical trials completed in the past 5 years using humans. Some of these may have been cited in the meta-analyses above.

1.Probiotics prevent Hirschsprung’s disease-associated enterocolitis: a prospective multicenter randomized controlled trial. (2015)

This RCT showed that treatment with probiotics significantly improved enterocolitis (inflammation of the small and large intestine) in children with Hirschsprung’s disease (a disease involving missing nerve cells of the colon and severe difficulty passing stool).

2. A randomized controlled trial to test the effect of multispecies probiotics on cognitive reactivity to sad mood. (2015)

This RCT showed that healthy people who supplemented with a specific multi-strain probiotic for 4 weeks had a reduction in “rumination” and “aggressive thoughts” as compared to a healthy control group. The authors suggested that that this warrants research for using probiotics to treat depression.

3. Effect of multispecies probiotics on irritable bowel syndrome: a randomized, double-blind, placebo-controlled trial. (2014)

This RCT showed that a specific multi-strain probiotic significantly improved IBS symptoms. After 4 weeks, 68% of the treatment group reported relief while only 37.5% of the placebo group reported relief. They also showed changes in fecal bacteria in the treatment group.

4. Influence of a combination of probiotics on bacterial infections in very low birthweight newborns. (2015)

This RCT compared 80 premature infants (under 33 weeks gestation). Half received a special combination of probiotics and half did not. In the treatment group, there were about half as many late-onset septic events and half as many late-onset infections as in the control group. Also, on average, the babies who received probiotics were discharged from the NICU earlier than those who did not.

5. The effect of probiotics on serum levels of cytokine and endotoxin in peritoneal dialysis patients: a randomised, double-blind, placebo-controlled trial. (2015)

This RCT showed that a 6 month probiotic treatment significantly helped dialysis patients maintain kidney function and reduce inflammation compared to the control group. I was unable to determine how significant the differences between groups were.

6. Effect of multi-strain probiotics (multi-strain microbial cell preparation) on glycemic control and other diabetes-related outcomes in people with type 2 diabetes: a randomized controlled trial. (2017)

136 participants with type 2 diabetes participated in a RCT to determine whether a specific multi-strain probiotic taken over 12 weeks could help control fasting insulin and HbA1c (average blood sugar). Researchers found the probiotics to be modestly useful. The effect did not reach clinical significance for HbA1c, but did for fasting insulin.

7. The Role of Probiotics in the Treatment of Dysentery: a Randomized Double-Blind Clinical Trial. (2017)

This RCT looked at how probiotics worked to help treat dysentery. The treatment group received a 7-strain probiotic for 5 days. They had significantly less time in the hospital and a shorter duration of bloody stools as compared to the control group. The effects were significant, but modest.

8. The Effect of Probiotics on Gut Microbiota during the Helicobacter pylori Eradication: Randomized Controlled Trial. (2016)

This RCT showed that H-pylori patients who received probiotics along with their antibiotic treatment had better success and reduced antibiotic-resistant gut bacteria.

9. Probiotics reduce psychological stress in patients before laryngeal cancer surgery. (2016)

This was a small study with only 20 patients who were randomly assigned to the treatment or control group. Researchers found that the patients treated with probiotics scored much lower on an anxiety test than the control group before they were to have surgery for laryngeal cancer.

10. Effects of continuous use of probiotics before liver transplantation: A randomized, double-blind, placebo-controlled trial. (2017)

This study divided 90 liver transplant patients into treatment and control groups. They found that the patients who were treated with probiotics prior to surgery had a much lower risk of infection after liver transplant. 90 days after surgery, only 5% of the treatment group had gotten an infection whereas almost 50% of the control group did.

11. Randomized controlled trial of probiotics after colonoscopy. (2017)

This RCT showed that probiotics modestly helped patients recover after colonoscopy. The treatment group reported pain for about 2 days after surgery while the control group reported pain for about 3 days.

12. Effect of probiotics on postoperative quality of gastric bypass surgeries: a prospective randomized trial. (2016)

This RCT looked at whether probiotic treatment could help GI symptoms after gastric bypass. 60 patients were divided into 3 groups: Probiotic A, Probiotic B, or digestive enzyme. Results were the same for all 3 groups. Their GI symptoms improved modestly after 2 weeks of any treatment. This study could not show that probiotics worked better than digestive enzymes.

13. Probiotics prevent hepatic encephalopathy in patients with cirrhosis: a randomized controlled trial. (2014)

This RCT compared 160 cirrhosis patients. The treatment group received probiotics for approximately 40 weeks while the control group did not. In that time, 7 patients in the probiotic group and 14 patients in the control group developed hepatic encephalopathy (brain damage caused by cirrhosis of the liver). Researchers concluded that the probiotics helped reduce hepatic encephalopathy.

14. Probiotics and prebiotic fiber for constipation associated with Parkinson disease: An RCT. (2016)

This RCT consisted of a treatment group (80 people) and a control group (40 people) who had constipation associated with Parkinson’s disease. The treatment group consumed fermented milk with pre and probiotics daily. After 4 weeks, the treatment group had significantly fewer constipation symptoms than the control group.

15. Probiotics and Child Care Absence Due to Infections: A Randomized Controlled Trial. (2017)

This RCT included 290 healthy children ages 8-14 months. Half were given a multi-strain probiotic for 6 months. At the end of the study, there was no difference in outcomes. Children who took probiotics were just as likely to get sick and need to be kept home as the control children.

16. Effects of fiber and probiotics on diarrhea associated with enteral nutrition in gastric cancer patients: A prospective randomized and controlled trial. (2017)

This RCT divided 120 patients undergoing gastric cancer surgery into 3 groups: fiber-free, fiber-enriched, and fiber plus probiotic enriched. After 7 days, people in the fiber plus probiotic group had significantly reduce diarrhea and other intestinal disorders compared with the other groups.

17. Effect of probiotics on the incidence of ventilator-associated pneumonia in critically ill patients: a randomized controlled multicenter trial. (2016)

This RCT evaluated 235 adults who were to receive mechanical ventilation for more than 48 hours. 36% of the treatment group acquired ventilator-associated pneumonia versus 50% of controls. Additionally, only 24% of the treatment group acquired pathogenic microorganisms whereas 44% of the control group did.

18. Probiotics (Lactobacillus gasseri KS-13, Bifidobacterium bifidum G9-1, and Bifidobacterium longum MM-2) improve rhinoconjunctivitis-specific quality of life in individuals with seasonal allergies: a double-blind, placebo-controlled, randomized trial. (2017)

This study divided 173 people with seasonal allergies into either the treatment or placebo group. After 8 weeks, the treatment group was experiencing significantly reduced allergy symptoms and improved quality of life.

19. Yogurt supplemented with probiotics can protect the healthy elderly from respiratory infections: A randomized controlled open-label trial. (2017)

205 volunteers age 45+ were divided into treatment and control groups. After 12 weeks, researchers determined that the risk of getting an upper respiratory tract infection was cut almost in half by taking probiotics.

20. Effect of probiotics on vaginal health in pregnancy. EFFPRO, a randomized controlled trial. (2016)

Researchers wanted to determine whether probiotic food supplements could maintain or restore normal vaginal microbiota during pregnancy. 320 pregnant women participated. The treatment group received probiotics during their first trimester. No significant differences were seen between groups.

What We Know and Don’t Know

Probiotics is a topic where there is a lot we still don’t know. The research I found is very promising, but also very incomplete. I could dedicate an entire blog to probiotic treatment for each condition for which they have been studied. Here, I will try to summarize my findings in a table. I’ll assign an efficacy category to each condition (Effective and well-studied, seems somewhat effective, or probably not effective) based on my research above. However, the 30 works I’ve cited may or may not represent the majority of the data (hopefully they come close). These were simply the most relevant reviews and clinical trials I found in my non-exhaustive search of Pub-Med abstracts.

Acute infectious diarrhea Effective, well studied
Antibiotic-associated diarrhea Effective, well studied
Clostridium difficile- associated diarrhea Effective, well studied
Hepatic encephalopathy Effective, well studied
Ulcerative colitis Effective, well studied
Irritable bowel syndrome Effective, well studied
Functional gastrointestinal disorders Effective, well studied
Necrotizing enterocolitis Effective, well studied
Acute pancreatitis Probably not effective
Crohn disease Probably not effective
Atopic dermatitis Effective, well studied
Dental caries Probably not effective
Gingivitis Effective, well studied
Cancer May be somewhat effective, not well studied
Constipation in children Probably not effective
Weight loss Probably not effective
Depression and Anxiety Found conflicting meta-analyses
Kidney function in dialysis patients Seems somewhat effective
Fasting insulin in diabetes patients Seems somewhat effective
Dysentery Effective, well studied
H-Pylori Effective, well studied
Infection after liver transplant Seems somewhat effective
GI symptoms after gastric bypass Seems somewhat effective
Constipation associated with Parkinson’s Seems somewhat effective
GI symptoms after cancer surgery Seems somewhat effective
As a preventative in healthy infants Probably not effective
Ventilator associated pneumonia Seems somewhat effective
Seasonal allergies Seems somewhat effective
Upper respiratory tract infection in ages 45+ Seems somewhat effective
Maintain healthy vaginal flora during pregnancy Probably not effective

Conclusions and applications

Each condition needs more research to determine exact strains and doses, whether probiotic foods are as effective as pills, and why treatments may work for some patients and not others.

As you can see from the table, probiotics have the best marks for GI related problems. Even for those, however, probiotics aren’t entirely understood.

Surprisingly, I did not find much research where healthy participants were studied using probiotics as a means to prevent illness or maintain health. The only study with truly healthy participants was the infant study, which found no differences between the treatment and control groups. This leads me to believe that probiotics are not a good idea at this time as an everyday supplement, especially since we have no guidance for which kinds and how much to take.

On the other hand, probiotics seem to be at least somewhat useful for a broad spectrum of illnesses and they don’t have many side effects for generally healthy people. There would be no physical harm for most people to take or eat probiotics just maybe to be on the safe side. I wouldn’t go spending a fortune though.

If you have a condition and are wondering whether to try a probiotic for treatment, I would highly recommend going straight to the peer reviewed research. Look for RCTs that have used probiotics for your specific condition. Since there is a lot we still don’t know about probiotics, it’s easy for supplement companies to promote unproven hypotheses for why and how they work or to cherry-pick studies. This is an area where you really need to consult the research instead of top websites.

I’m personally excited to see how much research is going into probiotics. We are slowly but surely figuring out the microbiome and how to help our little bugs improve our health.

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)

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: 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. This site keeps a list of quack physicians and links to help you understand why they can’t be trusted. This is a reliable source of information for all claims that need fact-checking. 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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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.


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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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. (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. (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. (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. (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. (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. (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. (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. (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. (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. (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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

This study found similar results to the studies above.

27. Effects of sodium fluoride on reproductive function in female rats. (2013)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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)

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!