Todd Allen

On Friday I ordered the 130X/30X WGS for $239 which gives results in about 8 weeks. I'm stunned at how quickly the prices have come down. At this price it seems an incredible bargain although I expect more accurate tests at even lower prices are coming. I wonder how long it will take to catch on and everyone will have a copy of their full genome? And how long it will take for it to be part of standard medical practice?

One thing I found interesting although bordering on ridiculous: While I have seen studies questioning how low to drive BP with meds I had yet to see a case where hypertension was considered beneficial. I wonder if they had stratified out hypotension from normotension would the hypertension group still fare best? My thinking being that after a heart attack or with heart failure low BP is likely a sign cardiac insufficiency. It would have been interesting to see the change in BP with the heart diagnosis/event. I suppose if one had a big drop in BP after a heart attack even if BP dropped into the normal range it might still be indicative of heart damage.

I think the explanation for why the two studies published in the same year have what look to be completely contradictory findings may be due to them actually looking at quite different things. The study I posted was looking at the rate of filed reports of ALS as an adverse outcome of having taken statins while your study is finding the number of people developing ALS declines with longer duration of statin use. So it might be that people more resistant to developing ALS are more likely to continue statin use for longer time periods versus those prone to ALS developing adverse reactions quickly and terminating statin usage. To answer the question of whether statins contribute to developing ALS I think a study that took a large cohort of people eligible for statin use and randomly selected half to forced statin usage and half to no statins and followed them until death would be more definitive. But that would be unethical.

Association between hyperlipidemia and mortality after incident acute myocardial infarction or acute decompensated heart failure: a propensity score matched cohort study and a meta-analysis And graphs showing the longevity benefits of hyperlipidemia and the higher the cholesterol the better the longevity after heart attacks or heart failure!

The systematic review of randomized controlled trials of PCSK9 antibodies challenges their “efficacy breakthrough” and “the lower, the better” theory

Or maybe "bad" cholesterol isn't so bad. Here is a study suggesting it is good for people with ALS. Dyslipidemia is a protective factor in amyotrophic lateral sclerosis

I'd like to hear his explanation of why ALS (the most common misdiagnosis for my disease SBMA) isn't a problem. Amyotrophic Lateral Sclerosis Associated with Statin Use: A Disproportionality Analysis of the FDA's Adverse Event Reporting System

Here's an excerpt:

Point: Why statins have failed to reduce mortality in just about anybody

Mine was low but when I started taking DMSA for lead poisoning my urinary levels for cadmium and a couple other metals jumped to somewhat alarming levels. Fortunately they have each dropped at roughly 10% per month of treatment and approaching a year of treatment only lead is still at a somewhat concerning level

Well I'm glad I waited. Dante Labs has just started a Black Friday sale for $149 30X WGS and $239 for 130X/30X. https://us.dantelabs.com/collections/advanced-dna-tests I think I'll wait a couple more days for any other Black Friday sales but I will be surprised if any beat this offer. This year anyway. At the rate prices have been falling this might be regular non sale pricing within another year or two.

Mine isn't so much a goal but just a rough estimate of where I expect to plateau. Here's a plot from a survey article at CholesterolCode suggesting my numbers are fairly average for people eating keto. It appears only the lean and athletic get LDL up in the 400-600 range. The highest I know of (without FH) is a woman who reported LDL labs in the mid 700s but she does power lifting competitions at single digit body fat % and I think was eating a beef only diet. Her LDL was 80 when her sport was running and she was chubby and eating high carb. Here a video interview with her back when her LDL was in the 400s. I think my high T is due to the expanded CAG repeat mutation of the androgen receptor gene which causes my disease SBMA. In clinical exams it is typically distinguished from ALS due to also causing signs of androgen insensitivity such as gynecomastia. I believe androgen receptor activation has a counter regulatory role on testosterone production. People with early stage SBMA still in good health tend to have mildly elevated T although it drops as the disease advances probably due to declining metabolic health. The first clinical trial of a drug therapy for SBMA was of testosterone supplementation and it accelerated neurodegeneration. I'm hoping my rising natural T in a context of improving health won't be as problematic. My gynecomastia is mostly gone and I am even growing some hair on my chest suggesting my body has found a level that compensates for the androgen insensitivity. A possible downside is that people with SBMA have low risk of prostate cancer and I might lose that benefit especially as I am trying hard to maximize IGF-1 with some success. I only had a few other hormone labs most recently: DHEA-SULFATE 195 mcg/dL 38 - 313 IGF-1 321 ng/mL 40 - 290 TSH 1.35 mIU/L 0.40 - 4.50 mIU/L and some consider this a hormone VIT D 25-OH TOTAL 57 ng/mL 30 - 100

Also from the abstract: They aren't actually testing anything. They are finding a correlation at a very coarse level. Additional observational studies confirming the correlation still wouldn't confirm causality.

I listened to it too. I think an oversight on their part was to not acknowledge that something like 88% of adults in the US (and most other westernized countries aren't too far behind) are insulin resistant with chronic hyperinsulinemia. A marker of this the triglycerides to HDL ratio. Numerous studies have shown that when this ratio is bad (>4) there is a significant correlation between LDL and CVD but when the ratio is good (<2) the relationship disappears. My ratio has dropped to ~0.8.

There are a bunch of genes that contribute to FH and it comes in many flavors. Some have exceptionally high LDL and no heart disease and excellent longevity. Other things have been found to correlate much better than LDL to early death from FH such as ferritin, homocysteine, clotting factors, markers of inflammation, etc. If your flavor of FH comes without any other high risk factors sweating over LDL might be unwarranted.