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Part 1.2: Obesity Risk, Nutrition, and Strong Misconceptions

Approx Reading Time: 10 mins

In light of the year of molecular shenanigans going on behind the scenes of my health, I decided it was time invest in one of the most true and basic forms of health assessment available (currently). Twas time for a genetic profile. Enter 23andMe, Dr Rhonda Patrick, and a whole lot of head scratching.

If you’re not assessing, you’re just guessing…

…and up until now, I was just guessing. I was judging my genetic heritage based entirely on what I saw with my own two eyes, what my parents had told me, and what I had understood to be occurring over time in my own health history. Granted, my health history is exorbitantly more complex than most, so my read on it may have been skewed.

At the end of this telomeric testimony, you’ll find a list of assumptions I held to be true, with their informed changes (if applicable). The list could go on and on, but these are some of the assumptions that have been addressed by a genetic profile and further investigations afterwards (there’s lots of resources out there, and even some services that will help you interpret your findings). Now, I am going to highlight some of the findings from my genome and what they will mean for my “Year To Fix It All” Project.

Gene: SH2B3, SNP Location: rs3184504

This gene is loosely associated with Celiac Disease, but it is much more complicated than that. One SNP is not enough to cause celiac, nor is even a constellation of SNPs. It just so happens that I have one in a list of many that are associated with celiac. When I correlate this finding with all others (or a lack thereof), as well as my my IgG Assay, I am confident to say that breads and gluten are not a must-remove, but may be of benefit to reduce (which is already how I behave). Outcome: Minimal Impact.

Gene: GSTP1, SNP Location: rs1695

This is one a meaningful one for me. People with this genotype may in fact be harmed by excess Vitamin E (especially alpha tocopherol). Wait, come again? Harmed from a Vitamin? This is the beauty of Genetics, they depict how our body reacts to out external/internal environment. Vitamin E is very typically a strong anti-inflammatory, antioxidant, and anti-atherogenic (meaning it typically helps decrease the likelihood of developing many forms of cardiovascular disease), even though the research has had a hard time proving efficacy in population studies. HOWEVER, in certain genotypes, it actually has the opposite effect, by raising the levels of pro-inflammatory cytokines in the blood. As we’ll talk about repeatedly, inflammation is extremely uncool in excess, so we generally want to keep that crap to a minimum. Outcome: Get all my Vitamin E from foods, watch supplements for excess Vitamin E.

Gene: FTO SNP Locations: rs9939609, rs17817449, rs1121980, rs1421085

If you had to pick one set of genes to have left alone, this would be it. The FTO gene, for lack of time to explain in more detail, is the one that controls just how fat you get, on average. In the nature vs nurture debate for going chubbo, the FTO gene is the main influencer on the nature side of the scale. If you’re all giggety-goo over this type of info, have a read about it HERE or just google that crap.

So, imagine my chagrin and frank surprise when 37% of my reported impactful polymorphisms from one database indicate that for me, this gene is, well, F-ed up. I could go into specific detail about each and every one of these SNPs, but here’s the bullet points on my SNPs:

  1. Associated with a 1.3-fold increased obesity risk. Saturated fat may have a negative effect on blood glucose and insulin levels and increases type 2 diabetes risk.
    • May benefit by having a higher polyunsaturated fat intake and a lower saturated fat intake.
  2. Intermediate increased risk of obesity and type 2 diabetes due to high production of ghrelin. Higher ghrelin levels are associated with over-eating due to lack of satiation.
    • Associated with obesity particularly in the context of a high saturated fat and low polyunsaturated fat intake.
    • May benefit by having a higher polyunsaturated fat intake and a lower saturated fat intake.
  3. Associated with a roughly 1.67-fold increased risk for obesity, particularly in the context of a high saturated fat and low polyunsaturated fat intake.
    • You’ve gotta be kidding me…67% higher risk of obesity!?!?!?! F…M…L.
    • May benefit by having a higher polyunsaturated fat intake and a lower saturated fat intake.
  4. Associated with a 1.3-fold increased obesity risk due to a shift from energy-burning adipocytes (brown adipose tissue) to energy-storing adipocytes (white adipose tissue). This results in adipocytes storing more lipids and more body-weight gain.
    • Also associated with reduced thermogenesis (the burning of fat to produce heat) in response to cold exposure and this genotype and may result in less fat burning in adipose tissue during cold exposure.  A possible way around this defect could be fish oil supplementation (checkout UCP1 if you’re really interested)
    • Has been shown to be attenuated by approximately 30% in physically active individuals.

So, as you can imagine, seeing all of this info hidden away in my genetic story gave me a pretty strong indication of one thing…Outcome 1: I am fit in spite of my genetics, not due to them. Outcome 2: I need to start being really intentional about keeping my saturated fat consumption under control and massively increasing my poly-unsaturated healthy fats. Also, the ketogenic diet would be nearly impossible for me to do well (more on this at later date).

*Side Note: I don’t know if this is an extrapolation, but I am willing to bet it is related. A month ago on a backcountry excursion into Valhalla Provincial Park, I was struggling. I was feeling really dizzy, light-headed, and massively overheated. This had become the norm for me in the last year of life, so I choose to go about my life anyway. Rest doesn’t seem to make it go away, or it does but only after a few hours. However, cold-immersion nearly stopped it in it’s tracks. After one particularly bad hike of about 30 minutes, I jumped into an alpine lake and sat down for about 20 minutes. When I stood up? Gone. I was like a new man, and the effects lasted for the rest of the day. I have since repeated this little dosage in many different times and places….and the effect is the same. It literally clears the dizziness and light-headedness within about 5 minutes of being in 70 degree ish water. So, Wim Hof Method, here I come.

This also makes me wonder about my strong preference for cold. I have had frost bite on my face a few times, love laying in the snow, and often find myself outside sans shirt in freezing conditions. I also can’t handle hot tubs and saunas, they feel like death to me. Anyway, back to our gene decode…

Gene: BDNF, SNP Location: rs6265

This gene codes for a thing called Brain Derived Neurotrophic Factor. As the name implies, it is very important. This little factor helps keep your nerves healthy, grows new ones, and makes sure you can learn new skills, as well as maintains part of your short term memory. So naturally, you don’t want it messed up.

So what’s a guy to do if it is indeed messed? Exercise…since people with my genotype typically have a lower amount of BDNF, and Exercise is one of the main ways to increase BDNF. But here’s an interesting kicker…this happens due to beta-hydroxybuterate, which is what you get in your system when you partake in the ketogenic diet or go into ketosis for other reasons….such as during fasting…which again, I will address later. Outcome 1: I need to exercise in order for my brain to work well, even more than the average person, and it probably wouldn’t hurt to do so in a fasted state or in the morning. More on this later as well.

But wait, there’s more! It just so happens that this genotype MAY be protective against social defeat and depression. HEY-O! We have a win.

Gene: JAK2, SNP Location: rs12340895

According to my profile, I have a 2-fold increased risk for cancers of the blood such as leukemia. This increased risk may be due to damaged hematopoietic stem cells that go on to form cancer stem cells.

So, if you’re a fan of Rhonda Patrick, or Valter Longo, or Dom D’Agostino, or Tim Ferriss or Jason Fung, you’ve probably heard about Intermittent Fasting (IF) or extended fasting. It just so happens that one of the largest benefits of fasting comes in the form of increased autophagy and apoptosis. And wouldn’t you know it,  Intermittent fasting and resveratrol (red wine) both have been shown to increase the clearance of damaged hematopoietic stem cells. Rock on. Outcome: Intermittent/extended fasting and I are going to become friends (for many, many reasons).

Gene: CYP2R1, SNP Location: rs2060793

This little SNP is a jerk. Why? Because having a kink in the genetic plans here makes it harder for me to convert the vitamin D that I get into it’s useful precursor format in my system. In case you haven’t heard, Vitamin D is ridiculously important to have as high as humanly possible (within reason), since having appropriate levels in your blood make you less likely to die of anything (all cause mortality). Yeah, not being dead is important.

Fortunately for me, I have had my Vitamin D tested and it seems to be fine (as of about a year ago). I supplement regularly with Vitamin D. Outcome: Plan to continue Vitamin D supplementation, while getting more and more non-hot sun exposure while I can.

Gene: FADS2, SNP Location: rs1535

I knew it! I knew I was a crummy candidate for being a vegetarian! When you have this genotype, you suck at converting ALA (alpha linoleic acid) into the crap you really need, eicosapentanoic acid (EPA). It’s on the magnitude of 1/3 worse. Since ALA is generally found in plants and EPA is generally found in animals, this means I am better at getting my brain candy (EPA) from animal sources! Yeeeeeeesssss!!!!! There’s a bit more to it than that, but I’ll leave it there. It’s not that I can’t eat the plants, but plant based foods that I would typically eat specifically because they offer lots of EPA (chia, flax, walnuts) are probably best left as “occasional” instead of “staple” foods. Outcome: I need to make sure I get my health fats from animal sources, and don’t go out of my way to get specific land sources.

Conclusion-ish:

I am going to assume that you didn’t actually read all of that. But if you did, I hope you learned a few things. I have one more genetics article under my belt, then we’ll move on to Part 2: Hormonal Indicators (Oooooo she gonna be exciting). In the meantime, here’s my conclusions from my assumptions above:

  1. I am lactose intolerant – TBD (later)
  2. I have great genetics for remaining skinny and appearing fit – UTTERLY FALSE
  3. I can eat whatever I want – UTTERLY FALSE
  4. “The South American Incident” is to blame for much of my body fat gain – FALSE
  5. I thrive on a high protein diet – TRUE! Hooray!
  6. I handle cold extremely well compared to most – Seemingly True!?
  7. I have high Alzheimers and Degenerative Neurological Disorder Risk –TRUE
  8. I have mental toughness and certain levels of stoicism from my upbringing – It may just be genetic after all.
  9. I have guts of steel (<10 incidents of vomiting in my life that I remember) – TBD.
  10. I thrive on confrontation – TRUE
  11. I thrive on tons of fish oils and Vitamin D – EXTREMELY TRUE
  12. I feel like trash when I don’t exercise – EXTREMELY TRUE
  13. I just straight up don’t feel amazing when I eat a lot of veggies – Unsure
  14. I could live off of meat alone, seriously – As long as it’s balanced with certain things, such as high PUFAs and Exercise
  15. I gas out extremely easy, and I mean extremely easy – Is FTO Gene my problem?
  16. I have no issues with gluten or breads – TRUE
  17. I am always starving, and hence could always eat, assumedly because of my high BMR, being skinny and all. – EXTREMELY TRUE. Apparently it’s hunger signals (ghrelin), not an actual high BMR. 
  18. I am not a morning person. – Will address later, but generally FALSE.

The point of this entire single nucleotide shemmozle is to inform my decisions going forward, so I can best suite a future of greatness and normal blood pressure. So, here’s what I am going to do.

Year To Fix It All Action Items -or- YTFIAAI!!!

(It’s pronounced like “eat fire”, only with intensity, like in the movies, as in “eat f-eye-ah”. As you may have guessed, I make things up a lot. *ahem* Lets eat some fire…)

  • Decrease use of exogenous saturated fats, like coconut oil and milk.
  • Increase consumption of fish and grass fed meats
  • Increase consumption of fish oils and other PUFAs (like olive oil)
  • Increase Vitamin D to previous supplementation levels
  • Get lots of sun, but preferably not in the heat, so mornings and evenings
  • Continue Intermittent Fasting (have been doing for about 2 months now)
  • Add in extended fasts (doing my 4th as I write this)
  • Exercise often at a high intensity (when possible, for obvious reasons) for beta hydroxybuterate reasons.
  • Continue cold exposure and systematize it. Lengthen time for cold.
    • Take Wim Hof Method in the next year (exciting news in the future for this one)
  • Don’t eat so much (my BMR is likely not as high as I thought)
  • Did I mention exercise!? I need to do more.

Next time out, we’re going to address mitochondrial function, nitric oxide needs, and…boners? I promise it won’t be as long next time. The blog, not the boner, that is.

3 thoughts on “Part 1.2: Obesity Risk, Nutrition, and Strong Misconceptions

  1. This was reading my own report. We share almost _ALL_ risk genes.
    If we ever meet, red wine (for the JAK2) is on me.

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