Inflammation gets a bad rap in the alternative health world: “Inflammation causes heart disease, cancer, and autoimmune disease! It’s at the root of depression.” These are all true—to some extent.

Name a disease, and inflammation is involved.

Crohn’s disease is inflammatory.

Major depression is inflammatory.

Heart disease is inflammatory.

Autoimmune diseases, which involve an inflammatory response directed at your own tissues, are inflammatory.

Arthritis is inflammatory.

Even obesity is inflammatory, with fat cells literally secreting inflammatory cytokines.

Yes, but the story is more complicated than that. Inflammation, after all, is a natural process developed through millions of years of evolution. It can’t be wholly negative. Just like our bodies didn’t evolve to manufacture cholesterol to give us heart disease, inflammation isn’t there to give us degenerative diseases.

So, Why Does Inflammation Happen?

When pain, injury, or illness hit, the first responder is the acute inflammatory response. In other words, it is brief, lasting several days or less. All sorts of things can cause an acute inflammatory response. Here are a few:

  • Trauma (punch, kick, golf ball to the head)
  • Infection by pathogens (bacterial, viral)
  • Burn (sun, fire, seat belt buckle on a summer day)
  • Chemical irritants
  • Frostbite
  • Stabbing/Cut/Laceration
  • Allergic reaction

Things happen pretty fast in an acute inflammatory response and involve several different players, including the vascular system (veins, arteries, capillaries and such), the immune system, and the cells local to the injury.

  1. First, something painful and unpleasant happens; choose one of the above injury options.
  2. Then, pattern recognition receptors (PRR) located at the injury site initiate the release of various inflammatory mediators, which in turn initiate vasodilation (or widening of the blood vessels). This allows increased blood flow to the injury site, which warms the site, turns it the familiar red, and carries plasma and leukocytes to the site of the injured tissue.
  3. The blood vessels become more permeable, thus allowing the plasma and leukocytes to flow through the vessel walls and into the injured tissue to do their work. Emigration of plasma into tissue also means fluid buildup, which means swelling.
  4. At the same time, the body releases an inflammatory mediator called bradykinin, which increases pain sensitivity at the site and discourages usage of the injured area. These sensations—heat, redness, swelling, pain, and a loss of function—are annoying and familiar, but they’re absolutely necessary for proper healing.

Why Is (Acute) Inflammation Essential?

Allow me to explain why the four primary symptoms of acute inflammation are necessary, despite being unpleasant:

  1. Increased blood flow warms the injury and turns it red, which can be irritating and unsightly, but it also carries the guys—leukocytes—that will be cleaning up the injury site, mopping up pathogens, and overseeing the inflammatory process.
  2. Swollen body parts don’t fit into gloves, are really sensitive, and don’t work as well as their slim counterparts, but a swollen finger is a finger that’s full of a plasma and leukocyte slurry and therefore on the road to recovery.
  3. Pain hurts, but if an injury doesn’t hurt and it’s serious, you’ll keep damaging it because you won’t know not to use it.
  4. Loss of function prevents you from using what could be one of your favorite body parts, but you don’t want to make it worse be re-injuring it. Besides, it’s only temporary.

What About Chronic Inflammation?

These symptoms both indicate and enable inflammation (and, thus, healing), but what’s the deal with inflammation being linked with all those chronic illnesses—like obesity, heart disease, and depression? How does something normal and helpful go haywire and become implicated in some of the most crushing, tragic diseases of our time?

When inflammation becomes chronic and systemic, when it ceases to be an acute response, when it becomes a constant low-level feature of your physiology that’s always on and always engaged, the big problems arise.

The inflammatory response is supposed to be short and to the point. And because a big part of inflammation is breaking the tissue down, targeting damaged tissue and invading pathogens, before building it back up, the inflammatory response has the potential to damage the body. That’s why it’s normally a tightly regulated system: because we don’t want it getting out of hand and targeting healthy tissue. But if it’s on all the time—if chronic inflammation sets in—regulation becomes a lot harder.

Acute vs. Chronic Inflammation

A perfect example of the acute inflammation versus chronic inflammation dichotomy is exercise.

A single hard workout raises inflammation. It’s a stressor, a damaging event imposed upon your body. See for yourself.

A hard run spikes C-reactive protein for up to two days.

During exercise, skeletal muscle releases the inflammatory cytokine IL-6, a marker of damage.

Volleyball practice elicits spikes in IL-6 in both male and female elite volleyball players.

Acute exercise spiked CRP in cardiovascular disease patients (but a four-month exercise program lowered it).

This table of inflammatory responses to strenuous endurance events shows some massive spikes in CRP, some up to 20-fold the baseline value.

Yet, study after study (epidemiological and clinical alike) shows that extended exercise programs generally reduce markers of inflammation (like C-reactive protein) over the long-term:

  • In elderly Japanese women, a 12-week resistance training program reduced circulating levels of inflammatory markers compared to baseline; reductions in CRP were associated with increases in muscle thickness.
  • American adults who engaged in frequent physical activity tended to have lower CRPs than adults who were more sedentary.
  • In type 2 diabetics, (key term coming up) long-term high intensity resistance and aerobic training reduced inflammatory markers over the course of a year (independent of changes in body weight, meaning activity was the key factor).
  • Endurance combined with resistance training reduced CRP in young, healthy women better than endurance training alone.
  • In obese, post-menopausal women, a basic moderate cardio program lowered CRP without really affecting body weight either way over the course of a year.

There are many more out there, but the general gist is that regular exercise tends to lower markers of systemic inflammation while acute exercise increases markers of acute inflammation. And sometimes what’s acute can become chronic. How do we make sense of this? How do we avoid making those acute spikes a chronic, constant thing?

Identifying Chronic Inflammation: Objective Markers

First, we need to be able to identify chronic inflammation. What symptoms and biomarkers can we use to track our inflammation levels?

CRP, or C-Reactive Protein

CRP is a protein that binds with dead and dying cells and bacteria in order to clear them from the body. It can always be found (and measured) in the bloodstream, but levels spike when inflammation is at hand. During acute inflammation caused by infection, for example, CRP can spike by up to 50,000-fold. CRP spikes due to acute inflammation peak at around 48 hours and declines pretty quickly thereafter (post acute-phase inflammation CRP has a half life of 18 hours). Thus, if the incident causing the inflammation is resolved, CRP goes back to normal within a few days. If it persists, the infection/trauma/etc. probably persists as well.

Highly sensitive to many different kinds of stressors, CRP rises in response to essentially anything that causes inflammation. This makes it valuable for determining that inflammation is occurring, but it makes it difficult to determine why that inflammation is occurring—because it could be almost anything. But if you’re looking for confirmation that you are chronically, systemically inflamed, an elevated CRP (in absence of any acute infections, injuries, burns, or stressors) is a useful barometer.

“Normal” CRP levels are supposedly 10 mg/L. Absent infection or acute stressors, however, ideal CRP levels are well under 1 mg/L. You want to stay well below 1; you don’t want “normal.” Between 10-40 mg/L (and perhaps even 1-9 mg/L, too) indicates systemic inflammation (or pregnancy), while anything above that is associated with real acute stuff. Note that exercise can elevate CRP, so don’t get tested if you’ve worked out in the last couple days.

IL-6, or Interleukin-6

T cells (type of white blood cell that plays a huge role in the immune response) and macrophages (cells that engulf and digest—also known as phagocytosing—stray tissue and pathogens) both secrete IL-6 as part of the inflammatory response, so elevated IL-6 can indicate systemic inflammation.

Tissue Omega-3 Content

This is a direct measurement of the omega-3 content of your bodily tissue. It’s not widely available, but it is very useful. Remember that anti-inflammatory eicosanoids draw upon the omega-3 fats in your tissues and that inflammatory eicosanoids draw upon the omega-6 fats. People having a higher proportion of omega-6 fats will thus produce more inflammatory eicosanoids. Now, we absolutely need both inflammatory and anti-inflammatory eicosanoids for proper inflammatory responses, but people with high omega-6 tissue levels make way too many inflammatory eicosanoids. Studies indicate that people with the highest omega-3 tissue levels suffer fewer inflammatory diseases (like coronary heart disease).

Research (highlighted and explicated here by Chris Kresser) suggests that omega-3 tissue concentrations of around 60% are ideal, which is a level commonly seen in Japan—the seemingly paradoxical land of high blood pressure, heavy smoking, and low coronary heart disease rates.

Omega-3 Index

This measures the EPA and DHA, the two important omega-3 fatty acids, as a percentage of total fatty acids present in your red blood cells. It doesn’t correlate exactly to tissue amounts, but it’s pretty good and a powerful predictor of cardiovascular disease risk. The omega-3 index doesn’t measure omega-6 content, but those with a low omega-3 index are probably sporting excessive omega-6 in their red blood cells.

Anything above 8% corresponds to a “low risk,” but levels of 12-15% are ideal and roughly correspond to the 60% tissue content mentioned by Chris’ article. Four percent and below is higher risk and can be viewed as a proxy for increased inflammation (or at least the risk of harmful systemic inflammation developing from normal inflammation).

Heart Rate Variability

I’ve written extensively on HRV in the past. Long story short, high HRV predicts lower levels of inflammation.

Systemic Inflammatory Response Syndrome Score

There’s the systemic inflammatory response syndrome, which is incredibly serious and has four criteria. If you have two or more of them at once, congratulations: you qualify—and should probably see a health professional immediately. This isn’t relevant for low-grade systemic inflammation, like the kind associated with obesity or autoimmune disease.

  • Body temperature less than 96.8 F (36 C) or greater than 100.4 F (38 C).
  • Heart rate above 90 beats per minute.
  • High respiratory rate, 20 breaths per minute or higher.
  • White blood cell count fewer than 4000 cells/mm³ or greater than 12,000 cells/mm³.

Of these objective markers to test, I’d lean toward CRP, HRV, and one of the omega-3 tests. CRP is pretty comprehensive, HRV is a two-fer (inflammation and general stress/recovery), and, while omega-3 tissue or blood cell content doesn’t necessarily indicate the existence of systemic inflammation in your body, it does indicate the severity of the inflammatory response you can expect your body to have. Taken together, these tests will give you an idea of where you stand.

Identifying Inflammation: Subjective Markers

There are also subjective markers. They may be harmless artifacts, but they may indicate that something systemic is going on.

Flare-up of Autoimmune Conditions You Haven’t Heard From In Ages

Sore joints, dry, patchy, and/or red skin, and anything else that indicates a flare-up. For me, this is usually mild arthritis.

Water Retention

Acute inflammation is often characterized by swelling at the site of injury. The same effect seems to occur in states of systemic inflammation, although they aren’t localized, but rather generalized.

Stress Load

If you feel stressed, you’re probably inflamed. I’m talking about the kind that has you rubbing your temples, face palming, sighing every couple minutes, and pinching the space between your eyes very, very hard.

Persistent But Unexplained Nasal Congestion

Could be allergies, sure, but I’ve always noticed that when I’m under a lot of stress and generally in an inflamed state, my nose gets clogged. Certain foods will trigger this, too, and I think it can all be linked to a persistent but subtle state of inflammation.

Overtraining

If you fit the bill for the eight signs of overtraining listed in this post, you’re probably inflamed.

Ultimately, though? It comes down to the simple question you must ask yourself: How do you feel?

I mean, this seems like an obvious marker, but a lot of people ignore it in pursuit of numbers. If you feel run down, lethargic, unhappy, your workouts are suffering, you struggle to get out of bed, you’re putting on a little extra weight around the waist, sex isn’t as interesting, etc., etc., etc., you may be suffering from some manner of systemic, low-grade inflammation. Conversely, if you’re full of energy, generally pleased and/or content with life, killing it in the gym, bounding out of bedlean as ever or on your way there, and your sex drive is powerful and age appropriate (or inappropriate), you’re probably not suffering from chronic inflammation.

Causes of Chronic Inflammation

We need to determine why inflammation is “on” all the time—and then take the steps to counter it. I’m going to fire off a few things that both induce inflammation and tend toward prevalence in developed countries. You let me know if anything sounds familiar to you.

  • Toxic dietsHigh-sugarhigh-processed carb, high-industrial fat, high-glutenhigh-CAFO meat, low-nutrient food is a pretty accurate descriptor of the modern Western diet.
  • Insufficient omega-3 intakeOmega-3 fats form the precursors for anti-inflammatory eicosanoids, which are an integral part of the inflammatory response. Poor omega-3 status means insufficient production of anti-inflammatory eicosanoids and a lopsided inflammatory response to normal stimuli.
  • Excessive omega-6 intake: Omega-6 fats form the precursors for inflammatory eicosanoids, which are an integral part of the inflammatory response. High omega-6 status (especially when combined with poor omega-3 status) means excessive production of inflammatory eicosanoids and a lopsided inflammatory response to normal stimuli. The more omega-6 you eat, the more omega-3 you crowd out for anti-inflammatory eicasonoid formation.
  • Lack of sleepPoor sleep is linked to elevated inflammatory markers. Poor sleep is a chronic problem in developed nations. Either we go to bed too late, wake up too early, or we use too many electronics late at night and disrupt the quality of what little sleep we get. Or all three at once.
  • Lack of movement: People lead sedentary lives, by and large, and a lack of activity is strongly linked to systemic, low-grade inflammation. People don’t have to walk to get places, they take escalators and elevators, they sit for hours on end, and they don’t have time for regular exercise.
  • Poor recovery: Other people move too much, with too little rest and recovery. When I ran 100+ miles a week, I certainly wasn’t sedentary, but I was chronically inflamed. Overtraining is a form of chronic inflammation.
  • Chronic stress: Modern life is stressful. Bills, work, commuting, politics, exercise that you hate – it all adds up and it doesn’t seem to let up or go away. And if it becomes too much for you to handle (I know it’s too much for me at times), your body will have a physiological, inflammatory response to emotional stress.
  • Lack of down time: When you’re always on the computer, always checking your email/Facebook/smartphone, you are always “on.” You may think you’re relaxing because your body is stationary, but you’re not relaxing.
  • Lack of nature time: We spend too much time contained in cubicles, cars, trains, and cities, away from trees, leaves, and soft earth. In a way, nature is home for us. Going home certainly has its measured benefits.
  • Poor gut health: The gut houses the bulk of the human immune system. When it’s unhealthy, so is your inflammatory regulation. A healthy gut is also selectively permeable, allowing beneficial compounds passage into the body and keeping toxins out. An unhealthy gut often becomes leaky, allowing toxins into the body to stimulate an immune, inflammatory response.
  • Poor acute stressor/chronic stress ratio: We respond far better to acute stressors than repeated, sustained stress – even if the latter is of a lower intensity.

See what I mean? Since we’re set up for acute stressors requiring an acute inflammatory response, all this other low-level, evolutionarily-discordant, superficially mild stuff set against a backdrop of misaligned fatty acid ratios and impaired gut health throws us off and sets us up for a lifetime of chronic inflammation.

Inflammation is a complex physiological process that can go wrong in a lot of ways. But luckily, sticking to the tried and true dietary and lifestyle measures will get you most of the way toward preventing inflammation from becoming chronic and untamed.

If you have any further questions about inflammation, fire away down below! Thanks for reading.

Primal_Fuel_640x80

References:

Eliakim A, Portal S, Zadik Z, et al. The effect of a volleyball practice on anabolic hormones and inflammatory markers in elite male and female adolescent players. J Strength Cond Res. 2009;23(5):1553-9.

Lara fernandes J, Serrano CV, Toledo F, et al. Acute and chronic effects of exercise on inflammatory markers and B-type natriuretic peptide in patients with coronary artery disease. Clin Res Cardiol. 2011;100(1):77-84.

Ford ES. Does exercise reduce inflammation? Physical activity and C-reactive protein among U.S. adults. Epidemiology. 2002;13(5):561-8.

Balducci S, Zanuso S, Nicolucci A, et al. Anti-inflammatory effect of exercise training in subjects with type 2 diabetes and the metabolic syndrome is dependent on exercise modalities and independent of weight loss. Nutr Metab Cardiovasc Dis. 2010;20(8):608-17.

Daray LA, Henagan TM, Zanovec M, et al. Endurance and resistance training lowers C-reactive protein in young, healthy females. Appl Physiol Nutr Metab. 2011;36(5):660-70.

The post The Definitive Guide to Inflammation appeared first on Mark’s Daily Apple.

Powered by WPeMatico

Dear_Mark_Inline_PhotoFor today’s edition of Dear Mark, I’m answering four questions from readers. First, should someone homozygous for the FADS variant that increases PUFA conversion eat less or more PUFA? Next, what’s the deal with all the mushroom coffees out on the market? Are they actually beneficial? Third, when looking for a healthy decaf coffee, what should you watch for? And finally, how should a breakfast skipper/intermittent faster deal with increased morning hunger caused by morning workouts?

Let’s find out:

I’m confused. I’m 75% Norweigan, the rest mixed european. My FADS (myrf) is homozygous. My genetic report says this variant has “higher than average levels of arachidonic acid, LDL and total cholesterol levels due to upregulated elongation of omega 6 PUFAs to pro-inflammatory compounds. Consider limiting sources of omega 6 PUFAs especially AA.” So this says PUFAs are bad for me because they are pro-inflammatory, but you are saying they aren’t bad because they get converted to Omega 3’s which are anti-inflammatory. Is this not the FADS gene you are talking about, but one of the others?

It is confusing, I agree.

If you have “upregulated elongation,” you should limit omega-6 PUFAs in the form of linoleic acid. A large amount of the linoleic acid you eat will be successfully converted to arachidonic acid, a precursor for inflammatory compounds. You’ll also be better at converting alpha-linolenic acid (ALA) to the omega-3s found in fish (DHA and EPA), but linoleic acid is a lot easier for most people to stumble across than ALA.

If you have “downregulated elongation,” you should still limit linoleic acid. Unconverted linoleic acid is fragile, unstable, and liable to oxidation. You don’t want it hanging around or being incorporated into your tissues. Nothing worse than a mitochondrial membrane loaded with linoleic acid.

The point is that in most ancestral diets, omega-6 PUFA in the form of linoleic acid was available in much smaller amounts than it is today. Industrialization has concentrated its availability in the food system. Today, we get seed oils in everything—baked goods, fast food, restaurant food, chicken and pork (from the feed). Back then, we had to remove nuts and seeds from their shells to get a dense crack at some linoleic acid. High levels of linoleic acid are bad for the carriers of all the various FADS alleles, just for slightly different reasons.

Great article as always Mark.

Just wondering about mushroom coffee? The type that includes reishi & other varieties supposedly high in immune boosting compounds. Any benefit?

Thanks,

Allia

We had the founder of Four Sigmatic, Tero Isokauppila, on the podcast awhile back. Interesting guy and a great line of products. His signature one is mushroom coffee.

Are there benefits?

Well, mushrooms are legit. You don’t even have to wade into the world of magical immunomodulatory, brain-nerve-regenerating, adaptogenic mushrooms to see some interesting effects. Common culinary mushrooms like brown, white, oyster, porcini, and chanterelle mushrooms may all produce major health benefits, including blood pressure regulation, nerve cell growth stimulation, immunomodulation, and cancer protection.

What about the mushrooms often included in these mushrooms coffees, like reishi, chaga, lion’s mane, and cordyceps?

Reishi: Stimulates the immune system, including a boost in natural killer cell and T-cell activity. It reduces fatigue in breast cancer patients and neuroasthenia patients (neuroasthenia is a confusing medical condition characterized primarily by fatigue, so this is a big effect). In potential colorectal cancer patients, it appears to reduce the number and size of adenomas (benign tumors that could presage the formation of less benign ones) in the colon.

Chaga: Full of phenolic compounds, many of which have anti-cancer potential. Reduces oxidative stress in patients with inflammatory bowel disease, even protecting against DNA damage.

Lion’s Mane: May reverse mild cognitive decline in the elderly, help people with nerve damage regenerate destroyed nerves and regain their ability to walk, and act as a nootropic in healthy people.

Cordyceps: Included with immunosuppressant therapy, helps kidney transplant patients improve kidney function and avoid kidney transplant side effects. Increases lactate threshold in elderly folks during exercise; an increased lactate threshold means you stay aerobic and burn fat for longer before relying more heavily on glycogen.

Coffee is legit, assuming you tolerate caffeine. And even if you don’t, decaf coffee remains a great source of phytochemicals.

Is “Swiss water process” all you need to look for in a decaf coffee to avoid all the nasty chemicals and solvents Mark talked about?

Yes, that’s all you need.

I have been intermittent fasting, last food around 8 or 9 pm and then not eating until around noon, and this has been working great. But I have added in a morning workout and now I am getting hungry sooner, sometimes right after the workout. I suspect I need to up my calories overall. Should I just go ahead and eat “WHEN” as you say, and not worry about the IF timing, or should I try to get more calories in during my current compressed window?

There’s value in both. I find it plausible that feeling the sensation of hunger—true hunger, as arises after a hard workout with very little in your stomach—is worth experiencing on a semi-regular basis. It’s a feeling humans are “meant” to feel, as our ancestral environments often dictated we go without food despite desiring (and even “needing”) it.

WHEN is also a valuable tactic. To eat when hunger ensues naturally is to honor your physiology. If anything is a valid and accurate indicator of your body’s immediate nutritional requirements, it’s your subconscious instincts and urges.

I’ll give a third option, too. Instead of skipping breakfast, why not skip dinner? Have your last meal at 4 or 5 PM, do your morning workout in a fasted state, break the fast at 8 or 9 AM right after. You could even follow a “eat only when the sun’s up” rule to make things simpler.

Good luck, and let me know what you decide to do.

That’s it for today, folks. Thanks for reading, and be sure to help out down below with your own comments and answers (and questions).

saladdressings_640x80

The post Dear Mark: PUFA Confusion, Mushroom Coffee, Swiss Water Process, and Timing the Fast appeared first on Mark’s Daily Apple.

Powered by WPeMatico

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!

phc_webinar_640x80

The post How Ancestry Might Inform Your Fat Choices appeared first on Mark’s Daily Apple.

Powered by WPeMatico