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