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Incidentally, one thing I’d currently like to be able to do is assess my calcium intake independently; being on a paleo-style diet (mostly for food intolerance reasons), the best UK (NHS) dietetic advice informs me that I must consume significant amounts of supplemental calcium or fortified ‘milk’, if not taking any dairy. Whereas nutritional advisors have reassured me that leafy greens are sufficient (and magnesium intake is more worthwhile supplementing).
I have low bone density (of the spine) as a minor concern, and am aware of the other known factors affecting this (from micro-nutrients to load bearing exercise).
Greens are high in calcium and is where I get most of my calcium. The micronutrient smoothie I make has a total of Here is my recipe.
Also, you may want to look into the vitamin D receptor polymorphism Bsm1 that is associated with low BMD (particularly in the spine). You get get a 23andMe test and use promethease to understand data. I discuss this here.
Also, vitamin K2 is important to make sure the calcium gets out of blood vessels and to the bone.
Hi, thanks for replying. My Vit D BSM (rs1544410) call is normal -/-, but serum D levels have tested low in previous years. I struggled to raise it much so am currently undertaking more assertive supplementation. Taking K2 and A in conjunction (plus vit C, Bs multi-mineral mix, etc, currently).
Regarding the smoothie:
[A] Why is there no stated magnesium in the flax milk section? Won’t that totally change the overall totals? (Also asked on YouTube.)
[B] How much of that calcium and magnesium, respectively might be expected in (well pressed) juice? I’m hesitant to consume that much (blended) fibre, given gut issues.
[C] May vegetable folate (folinic?) compete/interfere with active folate (methyl) supplementation. I’ve currently been trying dipping into the ‘Freddd protocol’ for my CFS.
Have you looked at your cypr21 that I mention in my report? This polymorphism is also associated with lower 25OHD.
Hmm…forgot about flaxmilk…I guess because people switch out what they use (flax, almond, coconut, water) I did not want to include that in my calculation.
Folate and folinic should be used in both pathways unless have MTHFR, in which case they would not compete.
CYP2R1 - I have 1 good, 1 homozygous bad, 1 no call. And I find the promethease report structure confused, so made my own custom report in LiveWello:
Image (colour coded report table, like genetic genie).
My report share (requires sign in).
Template (shared with community, hope that is ok).
I’m currently supplementing ~10000IU/day of D3, including emulsion drops and capsules. My serum levels peaked at 91nmol/L (36.4ng/L) after a summer of daily sun exposure and a winter of ~2000IU/day supplementation, have since fallen to 73nmol/L (1 year later without supplements). But just one of many things I’m working on currently.
Hmm…forgot about flaxmilk… I did not want to include that in my calculation
You appear to have included flax milks' calcium contribution, and (some of?) the other nutrients, but not the magnesium. Hence I pointed it out, because it greatly distorts the apparent overall balance in the total. (Spreadsheet malfunction?) I couldn’t find nutrition data for flax milk, however, but I assume there’d be a lot of magnesium, as in the seed form.
Erm, so methylfolate will compete with vegetable folate unless one has (homozygous?) MTHFR C677T (rs1801133) SNP?? (Freddd insists veg folate, and Folic acid, block active types for him (and others), although RichVanK seemed skeptical of generalising all those findings. Familiar with those two?)
Wow, those vitamin D levels seem low considering…
Magnesium is in flaxseed but I’m not sure how much is actually in flaxmilk. Would have to do some reading…
Folate from plants would NOT compete in anyone but folic acid could. Not familiar with any on the names you mentioned.
CRON-O-Meter (see the link above) should be an ideal tool do this.
@carlsonbjj This is very interesting…I’m going to try to get access to this paper. If it find anything, I’ll post it.
I would be interested to see some concrete findings too.
Yasko goes on about Comt(+/+) individuals having reduced tolerance to methyl donors. Maybe greater mood swings?
I’ve also seen Rich Van Konynenburg (on the Phoenix Rising forums) claim that a couple of his patients over-supplemented methylation supplements to the point they were clearing homocysteine so fast that their sulfation pathways were running dry.
Myhill seems to say that (for example) B12 is safe to the point you’d have to drown in it first… Although I’ve seen worries about mobilising metals to the brain or it getting oxidised (but then read enough and you’ll see every possible worry, it seems).
Personally, I felt that I ran into a limit with SAMe supplementation, but thought that was probably the sulphur aspect, having BHMT mutations and measured high cysteine, taurine, etc.
Original press release - microglia, brain localised excessive arginine degradation and suppressed immune state.
@KickAssBrockSamson @jwilson13 The microglia in the brain are like the resident macrophages, which require arginine for immune function. It has been shown that arginine consumption is much higher in the brains of Alzheimer’s patients compared to normal elderly. This makes sense because amyloid beta plaque accumulation activated microglia (activated microglia consume arginine). This results in a positive feedback loop because activated microglia causes more amyloid beta production. Starving the microglia of arginine would prevent them from being activated and thus stop the vicious cycle.
My concern is long-term effect. You are leaving the brain defenseless if microglia can NEVER become activated. It is similar to used steroids to treat inflammation. It works but with serious long-term consequences. I think that preventing the brain inflammation through other mechanisms is key here.
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