Yesterday, I linked to a study showing that the beneficial effects of high levels of cardiorespiratory fitness—the kind you build with cardio/endurance training, HIIT, and sprints—have no upper limit. At first glance, this study appears to bust the “myth” of chronic cardio and the U-shaped curve of endurance training and prove that the more you train, the longer you’ll live. This appears to run counter to some of my central claims—that too much mid-to-high intensity endurance exercise leads to burnout, health issues, and diminishing returns.

A commenter wrote a great comment that got me wondering:

As far as “the more exercise the better” study I wonder if folks who had to drop out of long distance cardio training due to injuries or cortisol driven exhaustion are considered in the equation? In other words, if you can tolerate chronic cardio you may live longer, otherwise it might break you down. Everyone has a sweet spot for exercising is my gut feeling and you have to “listen to your body”. I still like the primal mantra along the lines of (if I may be so presumptuous as to paraphrase Mark) “walk a lot, do sprints once a week, lift heavy things once or twice a week, spend time outdoors, take part in sports or recreational activities that are fun for you”.

What do I think is going on? How do the results of this paper jibe with my take on Chronic Cardio?

First off, we have to acknowledge the basic structure of the study.

This study didn’t actually measure “hours spent training.” They gave subjects treadmill tests (stress tests) to determine their cardiovascular fitness, then divided everyone into different tiers of fitness based on the results. In fact, the authors of the study criticized the shortcomings of previous studies which used self-reported training data instead of objective measurements of cardiorespiratory fitness like the treadmill test. This makes the study far more accurate and useful. It also means you can’t make any ironclad proclamations about the connections between hours spent training and longevity. You can certainly make inferences—people who had better cardio fitness probably spent more time training to get it—but there are other interpretations. All you can say for certain is that higher levels of cardio fitness predict greater longevity.

I don’t see how anyone could argue with that. Of course being fitter is better.

But my criticism of chronic cardio isn’t a criticism of cardiovascular fitness. It’s a criticism of how most people go around obtaining that fitness—by destroying their bodies.

That doesn’t have to happen anymore. Tons of top guys these days are finally figuring out that you don’t have to log as many laps/miles/etc as possible to maximize your performance, but that wasn’t always the case. I grew up convinced that the more miles I ran, the healthier I’d be. That’s how I did it back in my marathon and triathlon days, and it almost destroyed me and an entire generation of my peers.

You can train twice as much as the next guy yet have worse fitness, either because you’re not training intelligently, you’re overtraining and hampering the adaptive process, or you’re not sleeping. That’s chronic cardio. You can train less and get better results, if you’re optimizing your recovery, nutrition, and sleep. That’s Primal Endurance.

As for these subjects, there is some serious genetic confounding occurring. Those dudes with elite fitness levels well into their 70s are often a different breed. They’re hard to kill. They’re tough. They can withstand the discomfort of grueling mile after mile. What other types of discomfort can they bear and even grow from? They’re just more robust than the average 70-year-old. It may not be the elite training itself that’s making them resist death. It’s just as likely they have the genetic capacity to excel in endurance training, and even if they didn’t exercise they’d still live longer than average.

There’s also the healthy user bias. The kind of lifestyle regular exercisers follow emphasizes sleep, plenty of rest and recuperation, smart supplementation and nutrition, and all sorts of other things that are also linked to longer, better health.

This paper makes a strong case for using something like Primal Endurance to build great cardiorespiratory fitness without risking chronic cardio territory.

Thanks for writing and reading, folks. Take care!

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The post Dear Mark: Is There No Upper Limit to Endurance Training? appeared first on Mark’s Daily Apple.

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Many of you have asked about prostate health in a Primal context. Men are interested because they know men have a decent chance of getting prostate cancer. Women are interested because they’re worried about the men in their lives getting prostate cancer. Today, I’m going to delve deep into the topic, exploring the utility (or lack thereof) of standard testing, the common types of treatment and their potential efficacy, as well as preventive and unconventional ways of reducing your risk and mitigating the danger of prostate cancer.

Let’s go.

First, what does the prostate do, anyway? Most people only think about it in terms of prostate cancer.

It’s a gland about the size of a small apricot that manufactures a fluid called prostatic fluid that combines with sperm cells and other compounds to form semen. Prostatic fluid protects sperm against degradation, improves sperm motility, and preserves sperm genetic stability.

What Goes Wrong With the Prostate?

There are a few things that can happen.

Prostatitis

Inflammation of the prostate, usually chronic and non-bacterial. A history of prostatitis is a risk factor for prostate cancer.

Benign Prostatic Hyperplasia

Non-cancerous enlargement of the prostate. As men age, the prostate usually grows in size. This isn’t always cancer but can cause similar symptoms.

Prostate Cancer

What most of us are interested in when we talk about prostate health… After skin cancer, prostate cancer is the most common cancer among men and the sixth most common cause of cancer death among men worldwide. Yet, most men diagnosed with prostate cancer do not die from it; they die with it. The 5-year survival rate in the US is 98%.

That said, there is no monolithic “prostate cancer.” Like all other cancers, there are different grades and stages of prostate cancer. Each grade and stage has a different mortality risk:

  • Low-grade prostate cancer grows more slowly and is less likely to spread to other tissues.
  • High-grade prostate cancer grows more quickly and is more likely to spread to other tissues.
  • Local prostate cancer is confined to the prostate. The 5-year relative survival rate (survival compared to men without prostate cancer) for local prostate cancer is almost 100%.
  • Regional prostate cancer has spread to nearby tissues. The 5-year relative survival rate for regional prostate cancer is almost 100%.
  • Distant prostate cancer has spread to tissues throughout the body. The 5-year relative survival rate for distant prostate is 29%. Distant prostate cancer explains most of the prostate-related mortality.

What Are Symptoms of Prostate Cancer?

The primary symptom is problems with urination. When the prostate gland grows, it has the potential to obstruct the flow of urine out of the bladder, causing difficulty urinating, weak urine flow, painful urination, or frequent urination. This can also be caused by benign prostatic hyperplasia, a non-cancerous enlargement of the prostate.

What Causes Prostate Cancer?

A big chunk is genetic. People with “knockout” alleles for BRCA, which codes for tumor suppression, have an elevated risk of some forms of prostate cancer. That’s the same one that confers added risks for breast cancer.

Ethnicity matters, too. Men of Sub-Saharan African descent, whether African-Americans in the U.S. or Caribbean men in the U.K., have the highest risk in the world for prostate cancer—about 60% greater than other ethnic groups. White men have moderate risks; South Asian, East Asian, and Pacific Islander men have lower risks.

Testosterone has a confusing relationship with prostate cancer. Conventional wisdom tends to hold that testosterone stimulates prostate cancer growth, and there’s certainly some evidence of a relationship, but it’s not that simple.

In one study, men with low free testosterone levels were less likely to have low-grade (less risk of spreading) prostate cancer but more likely to have high-grade (higher risk of spreading) prostate cancer.

In another, testosterone deficiency predicted higher aggressiveness in localized prostate cancers.

In Chinese men, those who went into treatment with low testosterone were more likely to present with higher-grade localized prostate cancers.

Other studies have arrived at similar results, finding that “hypogonadism represents bad prognosis in prostate cancer.”

Many prostate cancer treatments involve testosterone deprivation, a hormonal reduction of testosterone synthesis. This can reduce symptoms and slow growth of prostate tumors during the metastatic phase, but prostate cancer tends to be highly plastic, with the ability to adapt to changing hormonal environments. These patients often see the cancer return in a form that doesn’t require testosterone to progress.

What About Testing?

If you have a prostate, should you get tested starting at age 40?

Not necessarily. The value of early testing hasn’t been established. Some researchers even question whether early testing is more harmful than ignoring it, and most of the research finds middling to nonexistent evidence in favor of broad testing for everyone. Early testing has a small effect on mortality from prostate cancer, but no effect on all-cause mortality.

PSA testing can also be inaccurate. PSA is prostate specific antigen, a protein produced by the prostate. It’s normal to have low levels of PSA present in the body, and while high levels of PSA are a good sign of prostate cancer—even years before it shows up in imaging or digital probes—they can also represent a false positive. Those two other common yet relatively benign prostate issues—benign hyperplasia and prostatitis—can also raise PSA levels well past the “cancer threshold.”

Other causes of high levels of PSA include:

  • Urinary tract infections
  • Recent sex or ejaculation
  • Recent, vigorous exercise
  • Certain medications.

In fact, if you have a PSA reading of 4 (the usual threshold), there’s still just a 30% chance it actually indicates cancer.

What About Treatment?

Let’s say you do have prostate cancer, confirmed by PSA and a biopsy (or two, or three, as needle biopsies often miss cancers). What next? Should you definitely treat it?

It’s unclear whether treatment improves survival outcomes. One study took men aged 50-69 with prostate cancer diagnosed via PSA testing, divided them among three treatment groups, and followed them for ten years. One group got active monitoring—they continued to test and monitor the status of the cancer. One group received radiotherapy—radiation therapy to destroy the tumor. And the last group had the cancer surgically removed.  After ten years, there was no difference among the groups for all-cause mortality, even though the active-monitoring group saw higher rates of prostate cancer-specific deaths (8 deaths—in a group of 535 men— vs 5 in the surgery group and 4 in the radiotherapy group), cancer progression, and metastasis.

In another study of men with localized prostate cancer, removing the prostate only improved all-cause mortality rates among men with very high PSAs (more than 10). In men with lower PSAs, “waiting and seeing” produced similar outcomes as surgery.

Prostate removal also carries many unwanted side effects, like incontinence and sexual dysfunction. No one wants prostate cancer, but it’s no small thing to have problems with urination and sex for the rest of your life. Those are major aspects of anyone’s quality of life.

Before you make any decisions, talk to your doctor about your options, the relative mortality risk of your particular cancer’s stage and grade, and how the treatments might affect your quality of life.

How Can You Reduce the Risk of Prostate Cancer?

1. Inflammation is definitely an issue.

For one, there’s the relationship between prostatitis, or inflammation of the prostate, and prostate cancer that I already mentioned above.

Two, there’s the string of evidence linking anti-inflammatory compounds to reductions in prostate cancer incidence. For example, aspirin cuts prostate cancer risk. Low-dose aspirin (under 100 mg) reduces both the incidence of regular old prostate cancer and the risk of metastatic prostate cancer. It’s also associated with longer survival in patients with prostate cancer; other non-steroidal anti-inflammatories are not.

Third, anti-inflammatory omega-3 fatty acids (found in seafood and fish oil) are generally linked to lower rates of prostatic inflammation and a less carcinogenic environment; omega-6 fatty acids can trigger disease progression. A 2001 study of over 6,000 Swedish men found that the folks eating the most fish had drastically lower rates of prostate cancer than those eating the least. Another study from New Zealand found that men with the highest DHA (an omega-3 found in fish) markers slashed their prostate cancer risk by 38% compared to the men with the lowest DHA levels.

2. The phytonutrients you consume make a difference.

A series of studies on phytonutrient intake and prostate cancer incidence in Sicilian men gives a nice glimpse into the potential relationships:

The more polyphenols they ate, the less prostate cancer they got.

The more phytoestrogens they ate, the more prostate cancer they got. Except for genistein, an isoflavone found in soy and fava beans, which was linked to lower rates of prostate cancer. The Sicilians are eating more fava than soy, I’d imagine.

How about coffee, the richest source of polyphenols in many people’s daily diets? It doesn’t appear to reduce the incidence of prostate cancer, but it does predict a lower rate of fatal prostate cancer.

3. Your circadian rhythm and your sleep are important.

Like everything else in life, tumor suppression follows a circadian pattern. Nighttime melatonin—which is suppressed if your sleep hygiene is bad and optimal if your sleep hygiene is great—inhibits the growth of prostate cancer cells and reduces their ability to utilize glucose. One way to enhance nighttime melatonin is by getting plenty of natural, blue light during the day; this actually makes nighttime melatonin more effective at prostate cancer inhibition. On the other hand, getting that blue light at night is a major risk factor for prostate cancer.

4. Get a handle on your fasting blood sugar and insulin.

In one study, having untreated diabetic-level fasting blood sugar was a strong risk factor for prostate cancer. Another study found that insulin-lowering metformin reduced the risk, while an anti-diabetic drug that raised insulin increased the risk of prostate cancer. Metformin actually lowers PSA levels, which, taken together with the previous study, indicates a causal effect.

5. Keep moving, keep playing, keep lifting.

This has a number of pro-prostate effects:

It keeps you insulin sensitive, so neither fasting insulin, nor fasting glucose get into the danger zone.

If you’re doing testosterone suppression treatment, exercise can maintain (and even increase) your muscle mass, improve your quality of life, and increase your bone mineral density.

Oh, and do some deadlifts. Men with prostate cancer who trained post-surgery had better control over their bodily functions, as long as they improved their hip extensor strength. If you don’t know, hip extension is the act of standing up straight, of moving from hip flexion (hip hinging, bending over) to standing tall. It involves hamstrings, glutes, and the entire posterior chain. Deadlifts are the best way to train that movement pattern.

The prostate cancer issue is frightening because it’s so common. Almost all of us probably know someone who has or had it, even unknowingly. But the good news is that most prostate cancers aren’t rapidly lethal. Many aren’t lethal at all. So whatever you do, don’t rush into serious treatments or procedures without discussing the full range of options in a frank, honest discussion with your doctor.

That’s it for today, folks. Thanks for reading. If you have any questions, comments, or concerns about prostate cancer, feel free to chime in down below. I’d love to hear from you.

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References:

Perletti G, Monti E, Magri V, et al. The association between prostatitis and prostate cancer. Systematic review and meta-analysis. Arch Ital Urol Androl. 2017;89(4):259-265.

Ilic D, Djulbegovic M, Jung JH, et al. Prostate cancer screening with prostate-specific antigen (PSA) test: a systematic review and meta-analysis. BMJ. 2018;362:k3519.

Brawer MK, Chetner MP, Beatie J, Buchner DM, Vessella RL, Lange PH. Screening for prostatic carcinoma with prostate specific antigen. J Urol. 1992;147(3 Pt 2):841-5.

Castro E, Eeles R. The role of BRCA1 and BRCA2 in prostate cancer. Asian J Androl. 2012;14(3):409-14.

Watts EL, Appleby PN, Perez-cornago A, et al. Low Free Testosterone and Prostate Cancer Risk: A Collaborative Analysis of 20 Prospective Studies. Eur Urol. 2018;

Neuzillet Y, Raynaud JP, Dreyfus JF, et al. Aggressiveness of Localized Prostate Cancer: the Key Value of Testosterone Deficiency Evaluated by Both Total and Bioavailable Testosterone: AndroCan Study Results. Horm Cancer. 2018;

Dai B, Qu Y, Kong Y, et al. Low pretreatment serum total testosterone is associated with a high incidence of Gleason score 8-10 disease in prostatectomy specimens: data from ethnic Chinese patients with localized prostate cancer. BJU Int. 2012;110(11 Pt B):E667-72.

Teloken C, Da ros CT, Caraver F, Weber FA, Cavalheiro AP, Graziottin TM. Low serum testosterone levels are associated with positive surgical margins in radical retropubic prostatectomy: hypogonadism represents bad prognosis in prostate cancer. J Urol. 2005;174(6):2178-80.

Banerjee PP, Banerjee S, Brown TR, Zirkin BR. Androgen action in prostate function and disease. Am J Clin Exp Urol. 2018;6(2):62-77.

Zhou CK, Daugherty SE, Liao LM, et al. Do Aspirin and Other NSAIDs Confer a Survival Benefit in Men Diagnosed with Prostate Cancer? A Pooled Analysis of NIH-AARP and PLCO Cohorts. Cancer Prev Res (Phila). 2017;10(7):410-420.

Russo GI, Campisi D, Di mauro M, et al. Dietary Consumption of Phenolic Acids and Prostate Cancer: A Case-Control Study in Sicily, Southern Italy. Molecules. 2017;22(12)

Russo GI, Di mauro M, Regis F, et al. Association between dietary phytoestrogens intakes and prostate cancer risk in Sicily. Aging Male. 2018;21(1):48-54.

Discacciati A, Orsini N, Wolk A. Coffee consumption and risk of nonaggressive, aggressive and fatal prostate cancer–a dose-response meta-analysis. Ann Oncol. 2014;25(3):584-91.

Dauchy RT, Hoffman AE, Wren-dail MA, et al. Daytime Blue Light Enhances the Nighttime Circadian Melatonin Inhibition of Human Prostate Cancer Growth. Comp Med. 2015;65(6):473-85.

Kim KY, Lee E, Kim YJ, Kim J. The association between artificial light at night and prostate cancer in Gwangju City and South Jeolla Province of South Korea. Chronobiol Int. 2017;34(2):203-211.

Murtola TJ, Vihervuori VJ, Lahtela J, et al. Fasting blood glucose, glycaemic control and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Br J Cancer. 2018;118(9):1248-1254.

Haring A, Murtola TJ, Talala K, Taari K, Tammela TL, Auvinen A. Antidiabetic drug use and prostate cancer risk in the Finnish Randomized Study of Screening for Prostate Cancer. Scand J Urol. 2017;51(1):5-12.

Park JS, Lee KS, Ham WS, Chung BH, Koo KC. Impact of metformin on serum prostate-specific antigen levels: Data from the national health and nutrition examination survey 2007 to 2008. Medicine (Baltimore). 2017;96(51):e9427.

Galvão DA, Taaffe DR, Spry N, Joseph D, Newton RU. Combined resistance and aerobic exercise program reverses muscle loss in men undergoing androgen suppression therapy for prostate cancer without bone metastases: a randomized controlled trial. J Clin Oncol. 2010;28(2):340-7.

Ying M, Zhao R, Jiang D, Gu S, Li M. Lifestyle interventions to alleviate side effects on prostate cancer patients receiving androgen deprivation therapy: a meta-analysis. Jpn J Clin Oncol. 2018;48(9):827-834.

Uth J, Fristrup B, Haahr RD, et al. Football training over 5 years is associated with preserved femoral bone mineral density in men with prostate cancer. Scand J Med Sci Sports. 2018;28 Suppl 1:61-73.

Park J, Yoon DH, Yoo S, et al. Effects of Progressive Resistance Training on Post-Surgery Incontinence in Men with Prostate Cancer. J Clin Med. 2018;7(9)

The post A Primal Guide to Prostate Health appeared first on Mark’s Daily Apple.

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A Primal woman’s first reaction to the prospect of taking synthetic hormone replacements for menopause? Probably a healthy dose of skepticism. We in the ancestral health community, after all, tend to view pharmaceuticals as a last resort—interventions that are overprescribed by vested interests, create their own set of side effects, and may even do more harm than good. To suggest that we “need” this or that prescription raises our hackles.

Besides, it’s not like menopause is a product of modernity or an aberration our ancestors never experienced; it’s a physiological stage that evolution has protected and selected in humans. It’s perfectly natural. Rather than the debilitating, miserable experience many women report having, menopause should be easier. Graceful, even. But it often isn’t.

And nature unfortunately doesn’t care about that. Menopause is nature’s way of preventing undue discomfort and reducing genetic damage to the group. Your average 50-year-old woman has a lot to offer the tribe in terms of wisdom, child care, and general know-how, but natural selection has also determined that it’s better for everyone if middle-aged women don’t easily get pregnant. Menopause achieves this by down-regulating the hormones and weakening the tissues necessary for conception. The problem is that these same hormones and tissues also figure prominently in a woman’s enjoyment of life and overall health.

What can happen when Mother Nature decides to step in?

  • Anxiety
  • Irritability
  • Loss of libido, vaginal atrophy
  • Night sweats
  • Hot flashes
  • Weight gain
  • Forgetfulness

Longer-term, menopause increases the risk of serious diseases like osteoporosis, heart disease, and breast cancer.

Those aren’t mere inconveniences. They can mar the beauty of what should be an enjoyable part of a woman’s life, interfering with her relationships, her productivity, her cognitive function, her sleep, and her basic ability to enjoy living.

Mother Grok didn’t take pharmaceutical hormone replacements, you might counter. She didn’t hit up the shaman for a compound blend of hormones, so why should you?

First of all, maybe she did. Pre-scientific peoples have been known to develop folk cures that seem primitive but end up getting scientific validation. Think of the medieval garlic-based concoction that we just found out can eliminate medication-resistant staph infections. Or the indigenous Amazonian tribes who somehow figured out if you brewed a certain vine with a certain leaf and drank the finished product you’d visit the spirit world, all without knowing the vine contained DMT and the leaf contained an MAO-inhibitor that made the DMT orally active. Or, to bring it back to menopause, the yam, which cultures have used for hundreds of years for menopause treatment without actually knowing it contains an estrogen mimetic with clinical efficacy.

Second of all, the basic Primal stance on pharmaceutical interventions is that they are useful and suitable when correcting a deficiency, a genetic proclivity, or an evolutionary mismatch—particularly when dietary and lifestyle interventions aren’t cutting it. If they can help us treat a condition that seriously impedes our life or pursuit of health, we should avail ourselves of the fruits of modern science. Hormone replacement therapy may very well qualify.

Philosophical qualms aside—does hormone replacement therapy (HRT) work? What factors play into its effectiveness—and safety?

First, Is It Safe?

This might just be the most contentious topic in medicine.

For decades, HRT was the standard treatment for postmenopausal women. Not only was it given to treat the symptoms of menopause, it was billed as an antidote to many of the chronic diseases that increased in frequency after menopause like breast cancer, osteoporosis, and heart disease. Most of this was based on observational data and small pilot studies. That changed with the Women’s Health Initiative (WHI), a massive series of randomized controlled trials involving tens of thousands of postmenopausal women. Finally, the establishment would get the solid backing they needed to continue prescribing HRT to millions of women for prevention of chronic disease.

Except it didn’t turn out so well. Midway through, they stopped the trial because they weren’t getting the desired results.

There were two different HRT study groups. In one study, women without uteruses either got placebo or estrogen alone. In the other, women with uteruses got a combo of estrogen and progestin (a progesterone analogue) or placebo. The estrogen was Premarin, a conjugated estrogen. The progestin was Prempro, or medroxyprogesterone acetate.

The E/P combo increased the risk of heart disease, breast cancer, pulmonary embolism, and stroke, and reduced the risk of colorectal cancer and fractures (but not enough to offset the increased risks).

The estrogen alone had no effect on heart disease (contrary to their hypotheses), but it did appear to increase the risk of stroke while decreasing the risk of breast cancer and fractures.

Following the publication and wide dissemination of the WHI results, HRT use plummeted among women. Breast cancer cases subsequently dropped by 15-20,000 per year. Hormone replacement therapy developed a bad rap that it has yet to shake.

Is it deserved? Yes and no.

While the WHI results highlight some very real risks associated with HRT, they don’t tell the whole story. There are other variables to consider when deciding on HRT.

How Early You Start Taking HRT Matters

Most of the women in the WHI study began HRT when they were very post-menopause: older, in their 60s and upward. They got worse results.

A much smaller proportion of the women in the study were under 60 when they started HRT. They had better results. In fact, among those women who initiated HRT before age 60, total mortality actually dropped by 30%.

Another analysis of the Women’s Health Initiative data found that women who started taking HRT during early pre-menopause were less likely to see the negative effects, like increased breast cancer and heart disease.

Another study found that older post-menopausal women taking estrogen took hits to their working memory that remained after therapy cessation, while younger post-menopausal women had no such reaction.

Women who took oral estradiol 6 years after menopause saw their subclinical atherosclerosis slow down. Those who took it later (10 years after) did not.

A recent large Cochrane meta-analysis found that while in general postmenopausal women taking HRT had a moderately increased risk of heart disease, breast cancer, and other diseases, a subgroup of healthy, 50-59 year old (so, younger) HRT users only had a slightly increased risk of venous thromboembolism.

The longer you wait to initiate HRT after menopause, the more adverse effects occur. Start earlier, if you do start

How You Administer the HRT Matters

Oral hormones have different metabolic fates than transdermal hormones. When you swallow a hormone, it goes to the liver for processing. This creates various metabolites with different bioactivity. One example is oral estrogen. When you take estrogen orally, you raise CRP, a marker of inflammation. Transdermal estrogen has no effect on CRP.

Oral HRT has been shown across multiple studies to increase the risk of venous thromboembolism, while transdermal HRT does not. This is because oral HRT increases thrombin generation and clotting, while transdermal HRT does not.

In the Women’s Health Initiative that found negative effects, the HRT given to the subjects was oral. Perhaps this was the issue.

For local vaginal symptoms, local application is probably ideal, while oral application is suboptimal. In one study, vaginal estriol was far more bioactive than oral estriol, despite the latter resulting in higher serum levels of the hormone.

However, topical isn’t always best. In one study, sublingual users of bioidentical hormones saw relief from night sweats, irritability, hot flashes, anxiety, emotional lability, sleep, libido, fatigue, and memory loss, while topical users only saw relief from night sweats, emotional lability, and irritability.

The Type Of Hormone You Take Matters

Another factor the WHI failed to address was the composition of the medication itself. They used synthetic hormones—conjugated estradiol and medroxyprogesterone acetate. Could bioidentical hormones, exact replicas of endogenous hormones which exploded in popularity following the WHI, have a different effect?

The amount of research into conventional HRT dwarfs bioidentical hormone therapy (BHT) research, but what we have looks pretty compelling.

Breast cancer is a major concern for HRT users. Most breast cancers respond to estrogen, just over half respond to progesterone, and traditional HRT seems to increase their risk. Yet, at least in healthy postmenopausal women, a combination percutaneous estradiol gel (inserted into the skin) and oral micronized progesterone—both bioidentical to their endogenous counterparts—had no effect on epithelial proliferation of the breast tissue, while reducing activity of a protein that protects cancer from cell death. The conventional HRT had the opposite effect, increasing epithelial proliferation and breast volume (a risk factor for breast cancer). This wasn’t about cancer, but it’s suggestive.

In another study, postmenopausal women on BHT (which included estriol, estradiol, progesterone, testosterone, and DHEA) saw improvements across all measured cardiovascular, inflammatory, immune, and glucoregulatory biomarkers despite being exposed to high levels of life stress.

Then again, in a recent study, bioidentical hormones performed poorly compared to the pharmaceuticals equine estrogen and medroxyprogesterone acetate. The pharmaceutical hormones resulted in a lower risk of breast cancer, although the bioidentical hormones still reduced the risk compared to placebo.

Which Hormones You Take Matters

The vast majority of postmenopausal women take estrogen, progesterone, or some combination of the two. But there’s another hormone that, despite plummeting during menopause, gets ignored—testosterone.

Although testosterone is the “male hormone,” it also plays a vital role in female physiology, especially sexual function. Menopause reduces testosterone by about half, and studies indicate that topical testosterone replacement therapy can improve sexual function and desire (combined with estrogen) as well as musculoskeletal health and cognitive performance in postmenopausal women. More importantly, topical testosterone improves sexual function without causing any of the adverse effects commonly associated with testosterone usage in women, like hair loss, voice deepening, body hair growth, facial hair growth, breast pain or tenderness, or headaches.

Adding low-dose testosterone to a low-dose estrogen regimen may even be better at reducing somatic symptoms of menopause (sleep disturbances, hot flashes, and other physical symptoms) than a higher dose of estrogen alone.

Your Expectations Matter

Our big mistake was treating HRT as a panacea for the chronic conditions of aging. It’s not that smart hormone replacement can’t or won’t reduce the risk of certain diseases, like osteoporosis or heart disease. It’s that we’re still figuring it out.

A better, safer move is to focus on what we know HRT can treat: the symptoms of menopause.

Want to reduce hot flashes and get more sleep? HRT works.

Want to reduce anxiety? HRT works.

Want to improve cognitive function and your sense of smell? HRT works.

The use of bioidentical hormones may be safer or more effective against the bigger stuff. It remains to be seen. Until then, treat symptoms, not chronic disease—but keep in mind your overall risks and discern whether treating the symptoms is worth any additional risk for that bigger stuff.

Your Personal Context Matters

Women with a history of estrogen-responsive breast cancer (80% of breast cancers) should exhibit caution and check with their oncologist before taking any kind of HRT.

ApoE4 carriers should seriously look into taking HRT. In one recent study, postmenopausal ApoE4 carriers exhibited rapid cellular aging—except if they were taking HRT.

Whatever You Decide…

Don’t feel guilty if you decide to take some form of it. I myself take a small dose of testosterone to get my levels up to where they should be. My wife, Carrie, has taken bioidentical hormones in the past (a modest compound blend of estrogen, progesterone, and testosterone) to deal with the symptoms of menopause, including persistent brain fog that didn’t respond to any other herbal or alternative measure in her case. There’s no shame. This is restoration of what’s healthy and supportive of a good life. 

Heck, I know women who are both aware of the potential long term risks—heart disease, breast cancer, and the like—and enthusiastic about the shorter-term, more immediate quality-of-life benefits they currently enjoy. They prefer the definite benefits over the small and uncertain absolute risk increases. Some have even said that feeling better day-to-day gives them the energy to continue living a healthy life in other ways.

I also know women who do the opposite, who either are lucky enough to not experience any profound symptoms in their transition or who prefer to use other methods and interventions to deal with their symptoms in order to avoid any increased long-term complications. (I’ll delve more into this in the future if there’s interest.) Regardless, it’s all a choice.

Hopefully after today you feel better equipped to make an informed one.

What about you, folks? I know I have thousands of readers who are facing this very question—or who have already faced it. What did you choose? How did you handle the HRT question?

Thanks for reading. Take care!

References:

Wu WH, Liu LY, Chung CJ, Jou HJ, Wang TA. Estrogenic effect of yam ingestion in healthy postmenopausal women. J Am Coll Nutr. 2005;24(4):235-43.

Murkes D, Lalitkumar PG, Leifland K, Lundström E, Söderqvist G. Percutaneous estradiol/oral micronized progesterone has less-adverse effects and different gene regulations than oral conjugated equine estrogens/medroxyprogesterone acetate in the breasts of healthy women in vivo. Gynecol Endocrinol. 2012;28 Suppl 2:12-5.

Ruiz AD, Daniels KR. The effectiveness of sublingual and topical compounded bioidentical hormone replacement therapy in postmenopausal women: an observational cohort study. Int J Pharm Compd. 2014;18(1):70-7.

Stephenson K, Neuenschwander PF, Kurdowska AK. The effects of compounded bioidentical transdermal hormone therapy on hemostatic, inflammatory, immune factors; cardiovascular biomarkers; quality-of-life measures; and health outcomes in perimenopausal and postmenopausal women. Int J Pharm Compd. 2013;17(1):74-85.

Zeng Z, Jiang X, Li X, Wells A, Luo Y, Neapolitan R. Conjugated equine estrogen and medroxyprogesterone acetate are associated with decreased risk of breast cancer relative to bioidentical hormone therapy and controls. PLoS ONE. 2018;13(5):e0197064.

Schiff I, Tulchinsky D, Ryan KJ, Kadner S, Levitz M. Plasma estriol and its conjugates following oral and vaginal administration of estriol to postmenopausal women: correlations with gonadotropin levels. Am J Obstet Gynecol. 1980;138(8):1137-41.

Scarabin PY. Hormone therapy and venous thromboembolism among postmenopausal women. Front Horm Res. 2014;43:21-32.

Espeland MA, Rapp SR, Manson JE, et al. Long-term Effects on Cognitive Trajectories of Postmenopausal Hormone Therapy in Two Age Groups. J Gerontol A Biol Sci Med Sci. 2017;72(6):838-845.

Hodis HN, Mack WJ, Henderson VW, et al. Vascular Effects of Early versus Late Postmenopausal Treatment with Estradiol. N Engl J Med. 2016;374(13):1221-31.

Santoro N, Allshouse A, Neal-perry G, et al. Longitudinal changes in menopausal symptoms comparing women randomized to low-dose oral conjugated estrogens or transdermal estradiol plus micronized progesterone versus placebo: the Kronos Early Estrogen Prevention Study. Menopause. 2017;24(3):238-246.

Yazici K, Pata O, Yazici A, Akta? A, Tot S, Kanik A. [The effects of hormone replacement therapy in menopause on symptoms of anxiety and depression]. Turk Psikiyatri Derg. 2003;14(2):101-5.

Doty RL, Tourbier I, Ng V, et al. Influences of hormone replacement therapy on olfactory and cognitive function in postmenopausal women. Neurobiol Aging. 2015;36(6):2053-9.

Jacobs EG, Kroenke C, Lin J, et al. Accelerated cell aging in female APOE-?4 carriers: implications for hormone therapy use. PLoS ONE. 2013;8(2):e54713.

Kingsberg S. Testosterone treatment for hypoactive sexual desire disorder in postmenopausal women. J Sex Med. 2007;4 Suppl 3:227-34.

Davis SR, Wahlin-jacobsen S. Testosterone in women–the clinical significance. Lancet Diabetes Endocrinol. 2015;3(12):980-92.

Achilli C, Pundir J, Ramanathan P, Sabatini L, Hamoda H, Panay N. Efficacy and safety of transdermal testosterone in postmenopausal women with hypoactive sexual desire disorder: a systematic review and meta-analysis. Fertil Steril. 2017;107(2):475-482.e15.

Simon J, Klaiber E, Wiita B, Bowen A, Yang HM. Differential effects of estrogen-androgen and estrogen-only therapy on vasomotor symptoms, gonadotropin secretion, and endogenous androgen bioavailability in postmenopausal women. Menopause. 1999;6(2):138-46.

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It appears that we’re well into “outrageous media frenzy over terrible or misleading claims by nutrition scientists” season….

Last week I covered the “low-carb” and mortality study, and for this week’s edition of Dear Mark I’m covering the (latest) coconut oil controversy. A Harvard professor recently launched a dramatic harangue against coconut oil, calling it “pure poison.” Is it true this time? Are we indeed killing ourselves?

Let’s find out:

Speaking of fat, I’d be interested in Mark’s take regarding the latest attempt to put the kibosh on consumption of coconut oil–specifically, a Harvard professor saying it’s pure poison, probably because it’s so heavily saturated.

I can’t stand the stuff, personally. I don’t like anything made with coconut, and it doesn’t like me either, possibly because I’m sensitive to the overload of lauric acid. However, this and many other websites tout coconut products as being super healthful.

So is there any truth to these new claims that coconut oil is actually bad for us? Is there any hard evidence that points to related health issues? Or is this just more of the same-old, same-old that we saw with eggs, red meat, etc.?

Here’s what Shary’s talking about.

I won’t even talk about the Tokelau, a Pacific Island people who obtained most of their calories from coconut. Or the Kitavans, who ate a relatively low-fat diet but got most of their fat from coconuts. Both showed pristine metabolic health, and in the case of the Tokelau, they actually got incredibly unhealthy after switching from their coconut-rich diet to one rich in mainland foods, including seed oils.

Nor will I talk too much about the animal studies, most of which have found favorable effects on health as a result of eating coconut oil.

Let’s just focus on the human trials—the intentional studies in which actual living humans ate coconut oil and then underwent lab tests to determine the health effects. Concrete, objective effects. If coconut oil is as toxic as this Harvard professor claims, the evidence should be overwhelmingly negative. A Harvard professor would never misrepresent the evidence, right?

First, there is 2017’s Effect of a Diet Enriched with Fresh Coconut Saturated Fats on Plasma Lipids and Erythrocyte Fatty Acid Composition in Normal Adults. Healthy adults either added coconut oil or peanut fat to their diet for 3 months, and researchers examined how the different fat sources affected their biomarkers. Coconut oil increased HDL levels and the proportion of an anti-inflammatory lipid subfraction in red blood cell membranes. All told, coconut oil had a neutral to beneficial effect on health.

2017 also had Physical Form of Dietary Fat Alters Postprandial Substrate Utilization and Glycemic Response in Healthy Chinese Men. As far as coconut oil’s toxicity goes, this one was a dud. Whether the men ate coconut oil or sunflower oil made no difference in their metabolic response to meals (though when the fats were in gel form, there was an effect).

Oh, but this one sounds negative: Coconut Oil Has Less Satiating Properties Than Medium Chain Triglyceride Oil. Finally! We’ve found a kink. Unfortunately, this one isn’t bad for coconut oil either. Although MCTs proved more satiating than coconut oil, the latter was still more satiating than the control oil—vegetable oil. This is actually a strong counter to the Harvard professor’s main contention that coconut oil is bad because it’s so high in saturated fat; MCTs are pure saturated fat and performed very well here. Also, most MCT oil products come from coconut oil.

Next is The Impact of Virgin Coconut Oil and High-Oleic Safflower Oil on Body Composition, Lipids, and Inflammatory Markers in Post-Menopausal Women.  There were no differences in body composition. Coconut oil raised total cholesterol, HDL, and LDL, but it was a wash. Both groups ended up with the same TC/HDL ratio (one of the best markers of overall heart health we have). One person had increased inflammation due to coconut oil, but most of the others had lower inflammation. Overall, though, the “impact of VCO and SO on other [inflammatory] cytokines varied on an individual basis.” The implication is that different people had different responses to the different oils. This is known, and it’s good to see researchers admit that people are different and the individual response arguably matters more than the statistical average of the responses.

In 2016, this came out: Postprandial serum endotoxin in healthy humans is modulated by dietary fat in a randomized, controlled, cross-over study. At first glance, it doesn’t look good for coconut oil. Compared to fish oil (which reduced it) and high omega-6 oil (which was neutral), coconut oil eaten with the meal increased the levels of serum endotoxin. Endotoxins are produced by bacteria in our guts and tend to increase systemic inflammation when they make it into our bodies. Coconut oil was pretty good at helping endotoxin make it past the gut and into the body. The good news is that this did not increase systemic inflammation—but keep in mind that these were “healthy humans.” An increase in serum endotoxins may have stronger effects on inflammation in unhealthy or obese humans. Another bit of good news is that pairing coconut oil with, say, fatty fish should mitigate any rise in serum endotoxins.

There’s also A Randomized Study of Coconut Oil Versus Sunflower Oil on Cardiovascular Risk Factors in Patients with Stable Coronary Heart DiseaseThe title tells it: patients with heart disease added either coconut oil or sunflower oil to their diets for two years. Researchers tracked basic risk factors and the number of “events,” or heart attacks. Despite people with actual heart disease eating the “worst” oil possible, “there was no statistically significant difference in the anthropometric, biochemical, vascular function, and in cardiovascular events after 2 years.” No difference.

Heck, according to 2016’s The Effect of Coconut Oil Pulling on Streptococcus Mutans Count in Saliva in Comparison to Chlorexidine Mouthwash, the coconut oil “myth” all the “experts” love to malign—that swishing coconut oil in your mouth can reduce harmful bacterial colonization—is actually true.

It’s obvious just from looking at these very recent studies, even some of the ones with negative or neutral effects, that coconut oil is far from poison. “Experts” do themselves no credit when they ignore and misrepresent the evidence like this.

Luckily, we can read for ourselves. And we can try for ourselves.

Thanks for reading, everyone. Thoughts on this coconut oil controversy—or other health related media hype? Other studies you’d like me to look at? Have a great week.

References:

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For today’s edition of Dear Mark, I’m answering a single, significant question. It concerns the latest “anti-low-carb” study claiming that we’re all killing ourselves by not eating bread. A reader wonders if the study is legit and if we should be worried about eating fewer carbs than “normal” people.

I don’t think we should be concerned, and I’ll explain why in detail. Let’s take a look and break it down.

Hi Mark,

I’m sure you’ve seen this latest study to claim that low-carb diets will kill us all: https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(18)30135-X/fulltext

Is it legit?

Yes, I’ve seen it.

Where to start?

This study came from Walter Willet, he of the voluminous mustache and unbridled enthusiasm for seed oils.

The most glaring weakness is the way they gathered the data. Over the course of 25 years, participants were asked to accurately report their diet reaching back as far as six years. This is an inherent issue in most nutrition data gathering, so it’s not unique to this study, but come on. Can you remember what you ate 6 years ago? Did your diet change at all, or was it stable enough to encompass with a curt summary?

The characteristics of the participants differed greatly.

Low-carbers were far more likely:

  • To be men—Males have a higher risk of mortality than women.
  • To be diabetic—Diabetes lowers lifespan, especially in the 1980s (when the bulk of the data was collected).
  • To be sedentary—Failure to exercise is a major risk factor for early death, and ill health in general.
  • To smoke cigarettes—Again, this is an elementary variable. Nothing like being able to smoke indoors. Remember smoking sections on airplanes? I do.
  • To eat fewer fruits and vegetables—Carnivory is popular these days, and may work for some, but plants are still good for you and actually complement a low-carb, high-meat diet quite nicely.
  • To be overweight—All else being equal, the fatter you are, the unhealthier you are.

Even if they were able to “control for” all those variables, you can’t control for the overall health and wellness trajectory of a person hellbent on ignoring their personal health. What other unhealthy things are they doing that weren’t captured and accounted for by the researchers?

For instance, alcohol intake. They didn’t look at alcohol intake in this trial. Seriously, search for “alcohol” in the paper and you’ll come up blank. It’s very likely that the low-carbers were drinking more alcohol, as similarly-conducted epidemiological research has found that “carbohydrate intake [is] the first to decrease with increasing alcohol consumption.” (2) Alcohol can take a serious toll on health and lifespan if you aren’t careful with your intake.

Oh, and low-carbers were also more likely to be on a diet. This might be the most crucial variable of all. Who goes on a diet, typically? People who have a health or weight problem. Who doesn’t diet? People who are happy with their health and weight. There are exceptions to this, obviously, but on a population wide scale, these trends emerge. Did the low-carb diet actually reduce health and lifespan, or did the health conditions that prompted the diet in the first place reduce health and lifespan?

Ultimately, this was all based on observational studies and epidemiological data. It can’t establish cause-and-effect, it can only suggest hypotheses and avenues for future research.

Luckily, we have controlled trials that demonstrate the health benefits of low-carb dieting, all of which correspond to better longevity:

You could make the argument that the positive health effects are purely short-term and that in the long run, those benefits turn to negatives. It wouldn’t be a very good argument, though, because we don’t have any indication that it actually happens. If you go reduce carbs or go keto and you lose body fat, gain lean muscle, improve your fasting blood sugar, normalize your lipids, and reduce inflammatory markers, I see no plausible mechanism by which those improvements lead you to an early grave. Do you?

It seems the burden of proof lies in the Willet camp. If the only healthy range of carbohydrate intake is between 50-55%, he would have to show that:

  • No healthy, long-lived cultures or individuals have a carbohydrate intake that strays from the 50-55% range. Anthropological and ethnographical evidence must confirm.
  • The benefits of low-carb diets, established through randomized controlled trials, are illusory and/or transitory, eventually giving way to health decrements that lower lifespan.

That’s a tough one. Hats off if he can pull it off. I doubt he can.

Thanks for writing in. I hope I allayed any concerns you might have had.

Take care, all, and be sure to share down below with your own comments and questions.

References:

1. Seidelmann, Sarah, MD, et al. Dietary Carbohydrate Intake and Mortality. Lancet. 2018. (Online First)

2. Liangpunsakul S. Relationship between alcohol intake and dietary pattern: findings from NHANES III. World J Gastroenterol. 2010;16(32):4055-60.

3. Thorning TK, Raziani F, Bendsen NT, Astrup A, Tholstrup T, Raben A. Diets with high-fat cheese, high-fat meat, or carbohydrate on cardiovascular risk markers in overweight postmenopausal women: a randomized crossover trial. Am J Clin Nutr. 2015;102(3):573-81.

4. Ballard KD, Quann EE, Kupchak BR, et al. Dietary carbohydrate restriction improves insulin sensitivity, blood pressure, microvascular function, and cellular adhesion markers in individuals taking statins. Nutr Res. 2013;33(11):905-12.

5. Rajaie S, Azadbakht L, Saneei P, Khazaei M, Esmaillzadeh A. Comparative effects of carbohydrate versus fat restriction on serum levels of adipocytokines, markers of inflammation, and endothelial function among women with the metabolic syndrome: a randomized cross-over clinical trial. Ann Nutr Metab. 2013;63(1-2):159-67.

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For today’s edition of Dear Mark, I’m answering six questions from readers. First, is funding from a biased source sufficient to negate a study’s results? Second, what are some good high intensity interval training workouts that people might not have considered? Third, what can someone recovering from an ACL tear do for HIIT without triggering knee pain flareups? Fourth, how do I like to eat spinach? And finally, how and when do I like to take collagen?

Let’s go:

On the nuts vs. carbs study, I want to say ‘follow the money’ since it was funded by the International Tree Nut Council Nutrition Research and Education Foundation. Then again, it was also funded by the Peanut Institute, so I don’t know what to think…

“Following the money” isn’t enough to come to any conclusions about the worth of a study. We can’t declare a study tainted based on bias alone, especially because we can’t avoid bias. Every person reading studies and deciding which one to write about is biased. Every organization meting out funding has biases. Every entity in the known universe has an agenda. It’s not “bad” (or good). It simply is.

If the cow consortium funds the “red meat is actually good for you” study, red meat is still good for you. The bias doesn’t negate the facts. Big Soy funds the “don’t worry about the quarter cup of soybean oil in your restaurant food” study, but it’s only a mark against the paper if the science was shoddy and the conflict of interest exerted influence (which it probably was and did).

But I totally understand where you’re coming from. There’s an entrenched bias against most of the health advice we support. The powers that be have spent decades telling us to avoid the sun, restrict meat (especially red meat), go vegetarian, eat low-fat, get “more complex carbohydrates,” use seed oils, do cardio over weights, eat less salt, and blindly drink more water. They’re not just going to go away—and they aren’t.

So whenever I see a study’s been funded by an obviously biased source, I can’t help but wonder and look more deeply at the paper with a skeptical eye. It sounds like you do the same. That’s great. It’s the kind of healthy skepticism we should all have and employ in our search for good information.

We just can’t stop there.

If the results  of a study are unfavorable to the funders, it’s a strong indication that the funding didn’t interfere with the science.

If the results are favorable to the funders, our hackles rise. We examine the study methods, design, and results to see if bias affected the results. Many times it doesn’t. Sometimes it does.

Can you point us in the direction of a good HIIT workout and what it should look like?

Here are a couple ideas:

Hill sprints. Find a hill and run up, then walk down. Walking down serves as active recovery. Steeper hills, shorter sprints with more rest. Hills with a gradual incline, longer sprints. All permutations work. Though extremely difficult, hill sprints are good options for many people with lower body injuries that flare up on flat ground sprints; running up a hill is gentler on your joints.

Barbell complexes. Pick 3-4 barbell movements. Clean and press for 5 reps. Romanian deadlift for 5 reps. Clean to shoulders, then front squat for 5 reps. Finish with 5 bent over rows. Do that without stopping or dropping the weight. That’s a complex. Drop the bar and rest a minute or two, then do another complex. Repeat. This works with any barbell movement, and you can even do kettlebell or bodyweight complexes. Adjust weight and reps accordingly. These complexes should be hard (but over quickly).

I tore my ACL 6 months ago. Although I am walking 5-7 miles a day and doing heavy lifting for my upper body. I am only able to do ball squats carefully at this point. Any HIIT ideas for me at this point? The bike causes pain on the front of my knee still.

Check with your doctor, but deadlifts are probably safe during knee rehab. Do them right and there’s very little knee flexion (it sounds like flexion hurts the knee); it’s all hip extension.

Deadlifts can become “cardio” if you drop the weight and increase the reps. Just maintain impeccable form. Don’t sacrifice technique (and back health) for a couple extra reps.

If you can deadlift safely for high reps without pain, the next thing to try is the kettlebell swing. Swinging a kettlebell is very similar to deadlifting a barbell—it’s all hip extension—and lends itself well to high-rep, HIIT-style workouts.

I’m one of few people I know who enjoys eating basically any type of offal (no problems with raw), but can’t handle spinach by itself. Any advice? Also, ever tried meditatin’?

And here’s where I’ll get thrown out of my own movement because of one of the ingredients.

Sauté spinach (frozen or fresh) in butter for a minute, add a handful of corn kernels (fresh or frozen, but organic or at least non-GMO), add salt, pepper, and dried chipotle pepper powder (as much as you can tolerate), cover, and turn heat to low. After about ten minutes, it’s ready. Finish with grated sharp cheddar or pecorino romano.

I don’t eat this often (never while keto), and it’s certainly not the only way I enjoy spinach. A good raw spinach salad is fantastic, as is basic sautéd spinach without the corn. But I’ve never met anyone who didn’t like the spinach-corn-chipotle recipe, even avowed spinach haters like yourself.

I’m curious about when Mark was supplementing heavily with collagen. Did he do that at breakfast as his only food, lunch in lieu of some other protein, a shake between lunch and dinner? What have other folks done?

I’m wary of too much protein in one sitting.

I would have 2-3 tablespoons of collagen with a little vitamin C half an hour before a workout. That’s been shown to increase collagen synthesis, a necessary step for healing tendons and other tissues.

That’s it for today, folks. Thanks for reading and take care!

Be sure to add your own comments, questions, and input down below.

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For today’s Dear Mark, I’m answering just one question from a reader. What are we to make of the new study purporting to show that saturated fat is the most harmful substance a liver can encounter? Should we remove all traces of it from our diets? Should we eat pure sugar? Quaff soybean oil? How relevant is an overfeeding study to a community of people dedicated to eating a sustainable, weight-reducing or -maintaining diet that includes saturated fat?

Let’s find out:

Hi Mark,

Did you see this study? http://care.diabetesjournals.org/content/early/2018/05/24/dc18-0071

What’s your take on it? Just got one of those classic emails from my vegetarian friend with only a link to the study and a smug emoji.

Oh yes, I knew this would come up after I linked to in on Weekend Link Love.

The title is “Saturated Fat is More Metabolically Harmful for the Human Liver Than Unsaturated Fat or Simple Sugars.”

I have a human liver. Do you? Probably. This is highly relevant to all of us, right?

Well, the first thing to understand is that this was an overfeeding study. Participants didn’t just eat a eucaloric diet with different energy sources. They each got a daily 1000 calorie snack on top of their normal diet for three weeks.

The SFA group ate 1000 extra calories in the form of butter, coconut oil, and blue cheese. The SFA:MUFA:PUFA ratio was 76%:21%:3%. Their liver fat increased by 55%.

The UFA group ate 1000 extra calories in the form of pecans, olive oil, pesto, and butter. Their SFA:MUFA:PUFA ratio was 21%:57%:22%. Their liver fat increased by 15%.

The Sugar group ate 1000 extra calories in the form of orange juice, soda, and candy. Their snack had no fat, all sugar. Their liver fat increased by 35%.

Saturated fat also increased lipolysis—the breakdown of fatty acids for energy—while unsaturated fat decreased it. Lipolysis normally increases during fasting or exercise. In that context, it’s a good thing and you end up losing body fat. If you have a steady stream of extra fat calories coming in, you won’t lose body fat. The researchers could have seized on this point and screamed “unsaturated fat inhibits lipolysis!” but they didn’t. Wonder why.

Also notable is the observation that overeating sugar increased de novo lipogenesis (creation of fat from sugar) in the liver by 98%. I was told that didn’t happen in humans, that de novo lipogenesis was a myth. Guess it can happen.

But, again, the most important thing to realize is that this was an overfeeding study. It wasn’t a weight loss study. It wasn’t designed to see which kind of diet spontaneously results in the most weight loss. It was designed to get people to eat 1000 extra calories from different nutrient sources to see how they affect liver fat. And they didn’t construct the entire diets around the hypothesis. From what I can tell, the participants ate their normal diets. Only the 1000 calorie overfeeding snacks were provided by the researchers.

You also have to consider choline. The more fat you eat, the more choline your liver needs to process that fat. In rats with fatty liver, supplementing with extra choline directly reduces liver fat. In Chinese women, a high choline intake protects against fatty liver. If the subjects didn’t increase choline as they increased fat overfeeding, they were bound to gain more liver fat. Remember: this was the whole point of the study.

Now with that out of the way, who is this study relevant for?

Those people who think keto gives them free license to consume as many calories as they can cram into their mouths. Don’t do that. Especially don’t do that with isolated sources of fat, including saturated fat. Overfeeding anything is bad news, unless you’re trying to gain lean mass, lifting hard and heavy on a regular basis, and the thing you’re overfeeding is whole food rather than isolated fat.

That’s it for today, folks. What are your thoughts? Does this study tell you anything new, or is it old news?

Let me know what you think down below. Take care, be well, and have a great day.

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inline Fiber.jpegThe tricky thing about fiber is that it’s not a monolith. There are dozens of varieties. Some of them perform similar functions in the body, but others have extremely unique effects. Some rend your colonic lining to stimulate lubrication. Some turn into gelatinous slurries. But we can’t talk about fiber without understanding that the word describes a variety of compounds. As such, anyone making declarative statements about “fiber” without differentiating between the different types and their effects isn’t being accurate (except for me in that exact sentence).

This leads to a lot of confusion. People make blanket statements that might be true for some types of fibers and incorrect for others. 

Today’s post will attempt to illuminate the bulk of the matter. I’ll go through some of the most common misconceptions and myths about fiber from all corners of the dietary world. Whether you’re keto, low-carb, vegan, carnivore, or breatharian, you’ll find something to love and hate in today’s post.

1) “Fiber makes you full.”

This is theoretically sound. Mechanoreceptors in the gut respond to physical fullness by triggering satiety hormones. Big loads of insoluble fiber increase intestinal bulk, while some soluble fibers can gel up and increase the size of the stuff moving through your gut. Both result in added pressure on gut mechanoreceptors.

How does it work in practice?

A review found that while soluble fiber reduced appetite more than insoluble fibers, the overall effect on body weight was quite small, unimpressive, and inconsistent. More recently, a soluble fiber supplement failed to have any effect on satiety hormones, appetite, and subsequent food intake for the first 150 minutes after eating in healthy adults. The plucky researchers aren’t giving in, however, promising “further research… to quantify how soluble fiber influences appetite several hours after consumption.”

Resistant starch, an indigestible type of starch that colonic bacteria ferment, on the other hand does appear to increase satiety in humans, reducing food intake by 15%.

2) “Every diet needs the same amount of fiber.”

As it turns out, fiber becomes more critical the more carbohydrates you eat.

Soluble fiber slows down digestion, reducing the rate at which energy is absorbed. This can be helpful for people with glucose intolerance or type 2 diabetes by slowing the release of glucose into the blood. 

The byproducts of fiber fermentation in the colon by gut bacteria often have beneficial effects on carbohydrate metabolism. Eating resistant starch, for example, lowers the postprandial blood glucose spike. This reduction may also extend to subsequent meals, indicating it’s honing your ability to handle glucose. Everyone can benefit from better glucose management, but it’s far more critical for people eating significant amounts of glucose.

3) “All the healthiest people studied eat fiber!”

Observational studies are fun and all, but they’re not a good way to prove the healthfulness of fiber. Looking at fiber intake is just about the best way to capture the “healthy user”—that person who does everything right, like walk daily, exercise regularly, abstain from tobacco, avoid binge drinking, and eat whole foods rather than refined ones. It doesn’t say anything definitive about the health effects of the specific dietary variable they’re observing.

That said, the fact that most healthy populations eat whole foods containing fiber indicates that fiber probably isn’t actively harmful.

4) “Fiber is just roughage for big impressive poops. No functional use.”

That’s mostly true of insoluble fiber, which is pure waste material that shreds your intestinal lining and increases stool volume.

There’s considerable evidence that people with type 2 diabetes can really benefit from prebiotic fiber supplementation:

  • Chicory-derived inulin, a potent prebiotic fiber, reduces liver enzymes and HbA1c, improves blood pressure and fasting glucose, and increases calcium homeostasis.
  • Inulin improves immune markers and glycemic control.
  • Resistant starch lowers insulin resistance and inflammation.

A review of studies found that while the prebiotic inulin reduces LDL-C (an imperfect biomarker of dubious utility) in all populations, only in type 2 diabetics does inulin improve HDL and blood glucose control. 

Prebiotic fiber may also help certain patients with non-alcoholic fatty liver disease (NAFLD). The usual therapy for NAFLD patients is weight loss. You lose enough body fat elsewhere and the fat you’ve accumulated in the liver starts to disappear, too.

What about lean NAFLD patients without any real weight to lose?

In lean patients with NAFLD, a synbiotic—blend of prebiotic fiber with probiotic bacteria—reduces liver fat and fibrosis by improving inflammatory markers. Pre-emptive consumption of prebiotics may even protect against the development of NAFLD.

Another function of fiber that occurs in everyone is the production of short chain fatty acids by gut bacteria. When gut bacteria ferment prebiotic fiber, they produce short chain fatty acids, many of which have beneficial metabolic effects.

Butyrate is the most important short chain fatty acid. It fuels colon cells and may prevent colon cancer. Its relationship with existing colon cancer cells is more controversial. Read more about that here.

One interesting line of research is studying the interaction between the ketone body beta-hydroxybutyrate and the short chain fatty acid butyrate. Initial indications suggest that the two may have synergistic effects on cognition, inflammation, and overall health. That alone may be a reason to make sure you get prebiotic fiber on your ketogenic diet, just to hedge your bets.

Now, might a low-carb or ketogenic diet work better for people with type 2 diabetes than adding fiber to their normal diet? Sure. Could such a diet reduce the need for fiber? Yeah, I could see it. The same goes for NAFLD—low carb diets are also excellent in this population. And perhaps people who aren’t eating so many carbs don’t need the short chain fatty acids to improve their metabolic function and insulin sensitivity. But the evidence for fiber in type 2 diabetes and NAFLD stands, and I suspect short chain fatty acid production matters even in low carb or keto dieters.

5) “Fiber cures constipation.”

It depends.

In one 2012 study, patients with idiopathic constipation—constipation without apparent physiological or physical causes—had to remove fiber entirely to get pooping again. Those who kept eating a bit or a lot of it continued to have trouble evacuating. The more fiber they ate, the worse their constipation (and bloating) remained.

A 2012 review found that while fiber may increase stool frequency, it doesn’t improve stool quality, treatment success, or painful defecation. Similarly, glucomannan, a soluble fiber, moderately improves defecation frequency in constipated kids, but has no effect on stool quality or overall treatment success.

However, galactooligosaccharides, a class of prebiotic fiber, do appear to improve idiopathic constipation. And inulin, another prebiotic fiber, improves bowel function and stool consistency in patients with constipation.

6) “Fiber aggravates gut issues.”

Some say fiber cures gut issues like IBS and IBD. Others say fiber aggravates them. Who’s right? Maybe both.

Both IBS-D (irritable bowel syndrome with diarrhea) and IBS-C (irritable bowel syndrome with constipation) patients can benefit from soluble fiber (psyllium) while insoluble fiber (bran) is far less effective.

Wheat bran works okay for IBS, if the patients can tolerate it. They tend to tolerate something like hydrolyzed guar gum much better.

For IBD, the evidence is mixed. One survey of Crohn’s patients found that those eating more fiber (23 grams/day) had fewer flareups than those eating less (10 grams/day), while colitis patients reported no difference in symptoms based on fiber intake.

On the other hand, studies indicate that a low-FODMAP diet, which eliminates most sources of fiber, especially fermentable prebiotic fiber, is an effective treatment for IBS and IBD. Low-FODMAP diets have been shown to reduce bloating, abdominal pain, quality of life, and overall symptoms in intestinal disorders.

These contrary results may not even be contradictory. If your gut’s messed up, one solution could be to add back in the fibers you’re missing. Another could be to take all the fiber out and start from scratch.

7) “Fiber reduces nutrient absorption.”

For a long time, the consensus was that fiber tends to bind with minerals in the gut and thus reduce their absorption. These days, researchers understand that many of these fiber-bound minerals become available after fermentation in the colon.

Another wrinkle is that dietary fiber often comes with phytic acid, which binds minerals and prevents their absorption. Take wheat bran. Often deemed “wheat fiber” and lambasted for its tendency to bind minerals, wheat bran isn’t just fiber. It’s also a significant source of mineral-binding phytic acid.

Prebiotics increase absorption of magnesium, heme iron, and calcium. This makes sense. Even if the prebiotics are binding minerals, they release them once they reach the colon for fermentation by gut bacteria.

Fiber may reduce absorption of plant polyphenols, however.

8) “No one needs fiber.”

On the surface, this appears to be a sound conclusion. The human host digestive system cannot digest it. The majority of the fiber we eat gets pooped out as literal waste material. Certain classes of fiber may improve our gut health, but no one is keeling over from a lack of fiber in their diet.

Some have argued that a sterile gut is ideal if you have the right diet, that employing vast hordes of gut bacteria is just an adaptive measure taken to deal with a substandard diet full of roughage. The problem is that most people throughout history and prehistory have eaten that roughage, employed those gut bacteria, utilized the metabolites those bacteria produce. I suspect thinking long and hard before you consider it immaterial to human health.

If that were true, why would breast milk—the only food specifically designed for human consumption—contain loads of indigestible oligosaccharides that feed the growing gut biome? Even if it turns out that feeding the gut biome is only vital during infancy, that’s still a population of humans who truly need fiber.

Here’s where I come down: Fiber is an intrinsic part of many whole plant foods (and even whole animal foods, if it turns out that our gut bacteria can utilize “animal fibers” like other top carnivores). The Primal-friendly plants, the ones our ancestors grew up eating approximations of, like fruits, vegetables, roots, and tubers, are mostly higher in soluble fiber and lower in insoluble fiber. The only way to get huge doses of insoluble fiber these days is with supplementation or by eating grains. I don’t suggest eating grains or supplementing with insoluble fiber. I do suggest eating fruits, vegetables, roots, and tubers (while managing your carbs).

As for the carnivore issue, I’m open to the possibility that a properly-constructed carnivorous diet (which may, remember, include gristly animal fiber) obviates the need for plant fiber, prebiotic or otherwise. I’m not confident enough to try it myself, though.

Do I think everyone should be supplementing with prebiotic fiber? No. I add inulin to my Primal Fuel protein powder, mostly to improve mouth-feel but also to feed beneficial microbes and increase butyrate production. I add prebiotic cassava fiber to my collagen bars, again to improve texture and feed gut bacteria. And I’ll sometimes use raw potato starch for its considerable resistant starch content, often just mixing it into sparkling water and drinking it straight. But for the most part, the fiber I eat is incidental to the foods I consume. Berries, non-starchy vegetables, jicama, garlic, onions, green bananas, nuts—these are all foods rich in fiber, particularly prebiotic fiber, and I eat a fair amount of them while remaining low-carb and often keto.

As you can see, the fiber story isn’t simple. At all. There are many variables to consider. If you’re confused and unsure of how to think about fiber, you’re on the right track.

What do you think, folks? How has fiber helped or harmed you? I’d love to hear from everyone.

Take care and be well.

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Inline Carnivore Diet.jpegAll-meat diets are growing in popularity. There are the cryptocurrency carnivores. There’s the daughter of the ascendant Jordan B. Peterson, Mikhaila Peterson, who’s using a carnivorous diet to stave off a severe autoimmune disease that almost killed her as a child. The most prominent carnivore these days, Dr. Shawn Baker (who appears to eat only grilled ribeyes (at home) and burger patties (on the go), recently appeared on the Joe Rogan Experience and Robb Wolf’s podcast, and is always breaking world records on the rower. Tons of other folks are eating steak and little else—and loving it. There are Facebook groups and subreddits and Twitter subcultures devoted to carnivorous dieting.

What do I think?

I’m no carnivore. I love my Big Ass Salads, my avocados, my steamed broccoli dipped in butter. My blackberries, blueberries, raspberries, and strawberries. My spoonful of coconut butter.

Yet, I get the appeal.

We’ve been eating meat for three million years. Its caloric-and-nutrient density allowed us to dispense with the large guts needed to digest fibrous plant matter and build massive, energy-hogging brains. There isn’t a traditional culture on Earth that wholly abstains or abstained from animal products. Nearly every human being who ever lived ate meat whenever he or she could get it.

Thus, meat appears to be the “baseline food” for humans. If you look past the cultural conditioning that tries to convince us that meat will give us heart disease, cancer, and diabetes, meat looks pretty damn good as a place to start.

The question is if it’s where we should stay exclusively…. 

All this said, I’m skeptical about the “steak and water” or “ground beef and water” diets of modern carnivory. Let me explain….

A Few Key Arguments For It (and My Feedback)

“In its natural state, meat is relatively safe as far as toxins go.”

Animals can run and bite and claw and fly to get away from predators; most don’t need to employ any chemical warfare that causes problems when you eat the meat. Sure, allergies and intolerances can arise, like if you get bitten by the Lone Star tick and pick up a red meat allergy, but those are quite rare.

“Whereas plants’ phytonutrients are pesticides.”

This is technically true. They are toxins the plant produces to dissuade consumption by predators—toxins that the plants manufacture to maim, poison, kill, or even just make life uncomfortable for the animals who eat it.

But just as we can do with many other “harmful” inputs, we tend to treat plant phytonutrients as hormetic stressors that make us stronger, healthier, and more robust. 

There’s an upper limit, of course. And many of the phytonutrients have been primarily applied either to populations eating normal omnivorous, often downright unhealthy diets or to unhealthy subjects trying to improve a disease marker. As I’ve said before, there aren’t any real studies in healthy human carnivores, so we don’t know one way or the other whether the promising results of the extant studies apply to people eating only animal products. 

“Meat nutrients are highly bioavailable.”

The protein has all the amino acids we need to live and thrive. We readily absorb and utilize the vitamins and minerals in meat; they already come in “animal form,” requiring little to no conversion before we can start incorporating them into our physiology. Plant nutrients usually undergo a conversion process before humans can utilize them, and not every human has the same conversion capacity.

Some of those essential and/or helpful nutrients only occur in meat, like creatine, carnosine, vitamin B12. There’s literally no realistic way to obtain them without relying on supplementation, which didn’t exist until the last hundred years.

“Nutrient requirement studies don’t apply to us.”

I could see that. They haven’t tested the requirements for selenium, magnesium, and iodine on a zero-carb carnivorous diet. Do they go down? Can you therefore get by and thrive on lower intakes—the low levels found in muscle meat?

It’s a tough call.

It hasn’t been empirically tested. That’s true. It largely hasn’t undergone a series of RCTs. You can’t pull up a Cochrane meta-analysis of carnivore studies. All we really have are anecdotes.

I’m not disregarding the power or relevance of anecdotes and testimonials. Those are real. They’re not all suffering from a mass delusion. They’re not all lying. Peer-reviewed? No. Admissible in a scientific paper? Not unless you call it a case study. When you’re there in the room with someone pouring their heart out because something you wrote helped them drop 50 pounds and reclaim their lives, you don’t go “Yeah, but where are the clinical trials?” At some point, the weight of anecdotes adds up to something substantial, something suggestive. And hey, if it’s working for you, there’s no arguing that. 

But I can’t point to anything solid and totally objective in the research. Not yet anyway.

Still, any time you embark on a historically unprecedented way of eating, whether it’s pure muscle meat carnivore or vegan, you should be a little more careful about what you think you know. 

What Do We Know About Carnivory in Human History?

We don’t know if there have been any purely carnivorous human cultures. We haven’t found any yet, and you can’t prove a negative, so I won’t say “there were none.”

In all the best candidates so far, though, plants sneak into the diets. The Inuit actually utilized a wide variety of plant foods including berries, sea vegetables, lichens, and rhizomes. They made tea from pine needles, which are high in vitamin C and polyphenols.  The Sami of Finland, who primarily live off a low-carb, high-fat diet of meat, fish, and reindeer milk (I have to imagine that’s coming to Whole Foods soon), also gather wild plant foods, particularly berries and mushrooms (Finland’s forests produce 500 million kg of berries and over 2 billion kg of mushrooms each year!), sometimes even feeding their reindeer hallucinogenic mushrooms to produce psychoactive urine. The Maasai are known for their meat, milk, and blood diets, but they often traded for plant foods like bananas, yams, and taro, too, and they cooked their meat with anti-parasitic spices, drank bitter (read: tannin- and polyphenol-rich) herb tea on a regular basis, and used dozens of plants as medicines (PDF). Even Neanderthals used plants as food and medicine, we’re learning.

Even if we discover evidence of carnivory in human prehistory or in some extant group, the emerging science of genetic ancestral differences suggests that the habitual diets of our recent ancestors shapes the optimal diet for us today. If your close ancestors weren’t carnivores, you might not have the adaptations necessary to thrive on an all-meat diet.

Still, what about Vilhjamjur Stefansson, an Arctic explorer who came away very impressed with the native Inuit diet and underwent a series of studies on the effect of an all-meat diet in man? He and a colleague did great for over a year eating only meat. But Stefansson wasn’t eating ground beef. In his own words, he ate “steaks, chops, brains fried in bacon fat, boiled short-ribs, chicken, fish, liver, and bacon.” Definitely carnivorous. Definitely not just steak or ground beef, as many modern carnivores seem to be eating. All those “weird” cuts gave him critical micronutrients otherwise difficult to get from just steak.

How To Best Optimize a Carnivore Diet

While you won’t find me switching to the carnivore side, if I were to do a carnivorous diet, here’s how I’d try to optimize it (and why).

Take Magnesium

A recent paper showed that the majority of people following a “paleolithic ketogenic diet” with at least 70% of calories from animal foods and including offal had adequate serum magnesium levels. That’s a great start. But earlier studies show that serum magnesium may not be the definitive marker. A person can have normal serum levels but inadequate tissue levels—and in the tissues is where magnesium does its work. A person can have normal serum levels but still be deficient.

Eat Eggs

They’re not quite animals, but they contain everything you need to build a bird from scratch. That’s cool·—bite-sized whole animal.

Eat Liver

Liver is unabashedly animal flesh. It absolutely qualifies for a carnivorous diet. Loaded with choline, folate, vitamin A, copper, and iron, it’s nature’s most bioavailable multivitamin. There’s no reason not to include it. If you get your hands on some fish livers, you’ll get a ton of vitamin D along for the ride.

  • There’s frozen liver tabs, where people dice up liver into little chunks and swallow them hole.
  • There’s liver smoothies, where absolute savages blend raw liver and drink it. I know a guy who fixed severe iron deficiency by drinking raw chicken liver orange juice smoothies, with the vitamin C in OJ meant to enhance iron absorption.
  • Liver is also great sauteed with fish sauce, citrus, salt, pepper, and sesame oil. Do it quick, don’t overcook.

Eat Seafood

A few oysters, some mussels, a filet of wild sockeye salmon… You’ll get vitamin D, long-chained omega-3s (which tend to rare even in pastured ruminant flesh), selenium, iodine, copper, iron, manganese. Not every meal has to—or should— be a New York strip. 

Implement Intermittent Fasts On a Regular Basis

A constant influx of muscle meat will keep mTOR topped up. That’s great for muscle growth and general robustness. Just do something to stop the protein intake for a day or two to  lest you start fueling unwanted growths.

Treat Spices and Other Low/Non-Calorie Plant Foods As Medicinal Supplements That Don’t “Count”

All the nearly-carnivorous cultures we have good data on did similar things, using bitter herbs and barks and the like as supplements to their diets. You’re not getting calories from this stuff. You’re getting non-caloric compounds that provide health benefits.

Get the Best Quality Meat You Can Find and Afford

While I’m sure a diet of snare-caught hare, Alaskan elk, and choice sockeye salmon you wrest from the grasp of picky grizzlies poised over rivers preparing for a long winter would be ideal, it’s not necessary. Yes, grass-fed and -finished/pastured as well as organic are ideal, but do the best you can with what you have.

Use Bone Broth

It’s a great way to get collagen and the glycine it contains to balance out all the methionine you’re eating, especially if you’re doing the muscle meat-only thing and avoiding most gelatinous cuts of meat.  Make it yourself or buy. Collagen supplementation, of course, works here, too.

The carnivore diet isn’t for me. I like plants way too much. But I’m cautiously optimistic that it could work for more people than you’d expect, provided they heed as many of my suggestions as possible.

That’s it for me, folks. What about you? Have any experience eating a carnivorous diet? Interested in trying? Let me know what you know!

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Inline_Ancestry Fat Choices.jpegOne of the more exciting developments over the past few years has been the explosion in population genetics research. People are a diverse lot, and even though we’re all people who essentially want the same things out of life (and we’re working with the same basic machinery), there’s a lot of wiggle room. It’s not just information for curiosity’s sake. The information researchers are uncovering about human ancestry can have real ramifications for how said humans should eat.

A couple years ago, I wrote a post laying out a few guidelines for using your personal ancestry to inform your diet. Today, I’m going to talk about another one: polyunsaturated fat metabolism.

For years, it’s been “common knowledge” in alternative health circles that most people just aren’t very good at converting the omega-3s (ALA) in plant foods into the long-chained omega-3s found in seafood (DHA, EPA), and that everyone should just eat fish for their omega-3s. This remains solid advice, but the reasoning needs a little tweaking. It turns out that the genes that encode the proteins responsible for conversion of ALA into DHA/EPA (and linoleic acid into arachidonic acid)—known as FADS—have a couple variants. Some variants make conversion less effective and some make conversion more effective. Furthermore, the distribution of these variants vary across populations.

For instance, the variant that increases conversion of ALA into DHA and EPA is more common in South Asian (Indian, Pakistani, Bangladeshi, Sri Lankan) populations and African populations than any other group, while it’s moderately common in Europeans and East Asians and rarest in Native Americans and Arctic natives. Why?

In Africa, anatomically modern humans initially crowded along the coasts because that’s where the food was, especially the omega-3-rich seafood that provided the nutrients necessary for brain expansion. When humans began expanding into the omega-3-deficient interior of the continent, those with the FADS gene variant for improved long chain PUFA conversion were more successful. They could live in areas totally bereft of marine foods and still make enough EPA and DHA to survive and produce big-brained babies. Researchers estimate that the new variant became entrenched in African populations around 85,000 years ago due to positive selection. To this day, African populations almost exclusively carry the variant that increases conversion.

Then, as modern humans left Africa and moved into Europe and Asia carrying that same genetic variant, they encountered new environments that placed new demands on their genes.

In South Asia, the gene variant persisted. Plants were plentiful and long-chained omega-3s were not due to warm water reducing the omega-3 content of marine life, and the ability to efficiently convert fats offered a survival advantage. About 3/4 of the population carries it today.

In East Asia, about 1/2 of the population carries it.

In Europe, meat and fish were more widely available. Conversion was less necessary when you had a regular intake of pre-formed EPA, DHA, and arachidonic acid. Thanks to European admixture with existing archaic populations who still had the conversion-decreasing variant, its frequency increased until the arrival of farmers from the East, whose agricultural innovations selected for and genes contributed to the conversion-increasing variant.

In Native American populations, including Arctic, North American, and Latin American natives, the variant is almost completely absent. They were getting all their long-chain PUFAs directly from animal and marine foods, and it shows in the genes.

That’s a broad overview. The story’s more complicated than that, of course. East Asia is a big place with many different ethnic groups. Same goes for Europe, and Africa, and everywhere else. Except for the Africans and Native Americans, the frequency of the variants vary within these populations.

In European populations, for example, the conversion-increasing variant has the strongest selection in southern European populations (Tuscans), slightly less strong selection in Iberian populations (Spain/Portugal), moderate selection in Britain and northern Europe, and the weakest selection in far northern Europeans (Finns).

The ancient European groups that fed into modern populations followed a similar north-south pattern of variance. West and Scandinavian hunter-gatherers in the north show the least selection for the variant, since the cold waters of northern Europe offered plenty of cold water fatty fish and elongation of plant omega-3s just wasn’t very helpful or necessary. Pastoralists and farmers to the south show the most selection.

What’s it all mean?

People with African ancestry are almost certainly homozygous (2 copies) carriers of the increased-conversion variant. South Asians, including Indians, Pakistanis, Bangladeshis, and Sri Lankans, are also strong candidates to be homozygous carriers. Southern Europeans are most likely heterozygous (1 copy) carriers, Western and Northern Europeans less so.

Indigenous ancestry (unless African) probably means you’re a carrier of the decreased-conversion variant. Alaskan or Greenland Inuit, American Indian, Mexican mestizo—they tend to have lower FADS activity due to the relatively recent inclusion of agricultural foods in their ancestral diets. The farther north your people hail from, the more likely you are to carry at least one copy of the decreased-conversion variant.

If you carry the FADS variant that increases conversion:

  • Watch your linoleic acid intake. A major reason linoleic—>arachidonic conversion was selected for was the rarity of both long-chain PUFAs and linoleic acid in the ancestral environment. Being able to convert all your linoleic acid to AA is great, assuming you’re not cooking with soybean oil, eating fries fried in corn oil, and snacking on potato chips in between meals. Seed oil high in concentrated linoleic acid is a historical aberration for everyone regardless of ancestry.
  • Don’t think you can skip the fish and start glugging flax oil just because your mom was Sri Lankan and your dad was Tuscan. Studies show that the benefits of long-chained omega-3s like DHA are not modified by FADS gene status. Everyone can benefit from fish. Some people just need it more.

If you carry the FADS variant that reduces conversion:

  • You need pre-formed DHA/EPA and arachidonic acid. You don’t make it very well. That means eating fish, shellfish, eggs, and other animal foods. Hard sell, I know.
  • And if you eat a ton of vegetable oil—as most people do these days—you’re in troubleResearch shows that people with the conversion-decreasing variant who eat a lot of linoleic acid have lower HDL, higher triglycerides, and a bigger waist than those who eat very little.
  • Your absorption and incorporation of DHA from food may be enhanced. One study in infants with the conversion-reducing variant found that taking fish oil increased DHA way more than in other babies. This could be a feature of infants with the variant—mom eats fish, passes DHA through breastmilk to baby, who absorbs every last drop—and not of adults.

Don’t know your FADS gene status? No problem. It’s actually more fun this way.

I would take the time to get your ancestry tested, unless you’re absolutely certain of your family tree—and it stretches far enough back to actually say something about your deep ancestry. That way you can look at the various populations from which you hail and make some educated guesses. And you can even plug the raw genetic data into a service that spits out your nutrition-and-health-related variants.

Even then, you may not get any hard and fast answers. FADS gene variant frequency data isn’t widely available for every possible ethnic group on Earth, so a lot of this is more art and intuition than hard science.

If the traditional diet of your immediate ancestry is plant-based—not vegan, just not buying steak from the non-existent grocery store—you probably carry at least one and perhaps two copies of the conversion-enhancing variant.

If your people lived near the sea or ate a decent amount of animal foods, you’re probably carrying one of the conversion-reducing variants.

Whatever you do, take it easy. Have fun with it. Very few people represent the tail end of an unbroken line of ethnic purity. Most people will vary a bit here or there, or a ton here and a ton there. I have a lot of Scandinavian ancestry, which explains my need for a lot of pre-formed DHA and EPA from wild seafood (I’ve confirmed with genetic tests).

As this topic is a moving target, with new data coming out constantly, I’ll probably revisit it from time to time. Until then, what do you all think about the field of ancestral influence and health? What’s your ethnic background, and what do you think it means for your ability to metabolize PUFA? And what other questions do you have regarding ancestry and diet?

Thanks for reading, everyone. Take care!

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