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background+blood work of someone new to CR with neuromuscular disease

Todd Allen

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The words "new" and "CR" seem like they don't really go together.  I'm in a weight loss phase.  If I achieve a low stable weight and maintain it with a low calorie nutritious diet then I think the term CR will be more fitting.


Anyway, I did 3 weeks of 1000 calories/day by going cold turkey on all high glycemic crappy carbs and greatly reducing much of the better carbs such as fruit too.  I then switched to roughly 1900-2000 calories/day to slow weight loss to roughly 1 lb/week.  I've been increasing consumption of better carbs such as fruit, sweet potatoes and quinoa.  Currently, I'm eating roughly 17% protein, 37% fat and 46% carbs and am meeting my basic nutritional needs as checked by CRON-O-METER, except for modest deficiencies of B12 and D for which I take supplements.  I'm 5'10" and my weight had dropped from 174 to 161 lbs at the time of my most recent blood tests and I'm continuing to lose a pound/week which I plan to sustain until I've lost my pinchable fat which ought to take me to 130 lbs or maybe lower.


I was drawn to CR as potentially therapeutic for my inherited neuro-muscular disorder SBMA, aka Kennedy's disease.  I also have poor biomarkers for CVD and was hoping for improvement.  My mother suffered terribly from numerous strokes in her 50s and 60s and in April I lost a friend with SBMA only a little older than myself, 51, to a stroke which moved me to action.  My resting pulse and blood pressure have been improving quickly.  BP is down about 25 points and lately is in the range of 120-130/80-90.  I've also been exercising, improving rapidly from being barely able to walk to walking rough 3  miles/week, bicycling 30 miles/week and doing ~10 hours/week of other exercise mostly indoors.  For a couple weeks I was exercising in all forms for a much greater number of hours but I stopped making gains.  Incorporating longer periods of rest  between exercising I'm making good gains again.


I got blood test results on Friday and spent some time this weekend trying to understand them. Here are my results and current thoughts.


CPK 1432, 1144 6 mo ago, ref range 9-185 U/L
This is an indicator of muscle damage, I was hoping my change in diet and supplements would minimize the increase with resumed exercise. I was at 1760 a few years ago when I stopped exercising and far higher in my early 30s when I exercised vigorously and was doing 100 mile bicycle rides. My loss of muscle since then may be the reason it hasn't risen as high this time, or maybe the combination of things I'm doing now is helping a little.

aldolase 16.2, 18.2 2 yrs ago, ref range 2-8 U/L
This is another indicator of muscle damage. It's an enzyme found in muscle involved with glucose metabolism. The dropping level might be a sign that my regimen for addressing SBMA is helping or it might merely be an indication of my diet shifting me towards metabolizing more fatty acids and less glucose. I need to find guidance to better understand this.

Testosterone binding globulin, 81, ref range 10-80 mmol/L
Testosterone accelerates SBMA, my mother had high testosterone and developed significant symptoms of SBMA in her late 40s. I had a previous test a few years ago which also showed me above the reference range. I've been told testosterone fluctuates and individual tests aren't that meaningful.  I was hoping my diet would have lowered it more and perhaps it eventually will.  I'm going to push this strongly now with my doctors to further evaluate and hopefully come up with a way to get my level to the bottom of the reference range or lower. Dutasteride, a testosterone antagonist, is a drug that has been trialed for SBMA that I believe was shown to be modestly beneficial. I'll look into it more closely and try to decide if the benefits might outweigh the risks in my case.

human growth hormone, <0.1, ref range <10.8 ng/mL (they noted checking this twice to rule out making an error)
HGH may slow SBMA. In a study of a mouse model of SBMA growth hormone (I think IGF1 specifically) was shown to promote muscle regeneration and preserve nerve function. I wasn't expecting this result though it might explain a lot. I've long felt I've had little capacity to recover from injury. When my wisdom teeth were extracted a lingual nerve was bruised resulting in a burning sensation in my tongue. The surgeon said this was common and would resolve in a couple weeks, but 15 years later it has only subsided from a fierce burning to a mild burning. And strenous high intensity activity such as body building style weight lifting or any exertion that results in deep muscle strain can take 2 or 3 weeks to recover instead of the 2 or 3 days that it should. I know human growth hormone is used therapeutically for some conditions and I need to find out if it is appropriate for me though too much is associated with cancer and other aging related issues.

MCV, 96.6, 93.2 6 mo ago, ref range 81-99 fL
This is a measure of the size of red blood cells. High results can be an indicator of macrocyctic anemia a condition that can develop in response to a B12 deficiency. A few years ago I was found to have a severe B12 deficiency which was immediately addressed by a series of injections. And followed that with an oral B12 supplement for maintenance. My neurologist was deeply alarmed as B12 deficiency causes neurological damage that untreated can become so severe it results in death. B12 is found in animal based food products such as meat, fish, eggs, dairy, etc. I had been eating mostly vegetarian for decades for ecological reasons and thinking without doing any research that I was eating relatively healthy and was oblivious to the risk of B12 deficiency without supplementation. I had read that vitamin supplementation in general is unneeded for those with good diets and assumed I was doing ok.  And for years I was developing neuropathies consistent with B12 deficiency that my doctors and myself assumed was somehow related to SBMA and failed to properly investigate. My doctors knew I was eating mostly vegetarian and still failed to find this for a very long time.  The supplement I take is 500 mcg which claims is 8000% of the rda.  It seemed ridiculously high so I faded back to taking it roughly once/week. With the tests showing my MCV value is again rising I'm going back to once/daily.

MCHC, 33.3, 34.9 6 mo ago, ref range 32-35 g/dL
When high it is another potential indicator of B12 deficiency, so I'm glad to see it falling and it might indicate increasing B12 supplementation is not needed. Supposedly there is little to no risk with supplementing B12 at too high a level so it seems most prudent to go back to the higher level for now.

WBC, 7.4, 6.8 6 mo ago, ref range 3.5-11.0 10*3/uL
RBC, 5.22, 5.17 6 mo ago, ref range 4.47-5.91 10*3/uL
hemoglobin, 16.8, 16.8 6 mo ago, ref range 13.5-17.5 g/dL
hematocrit, 50.4, 48.2 6 mo ago, 41-53%
RBC dist width, 13.1, 13.2 6 mo ago, ref range <14.3%
platelet count, 265, 254 6 mo ago, 150-450 10*3/uL
mean platelet volume, 12.0, 11.7 6 mo ago, ref range 9.0-12.6 fL
All are ok?

albumin, 5.2, 4.9 6 mo ago, ref range 3.5-5.0 g/dL
Increased blood albumin may be due to dehydration or a high protein diet. I've boosted protein intake and increased it as a percentage of my diet by reducing carbohydrates in an effort to retain lean muscle mass while dieting to lose fat.   I only drink water now and I'm drinking a lot more, still I think the rising albumin is an indicator more of dehydration than protein as I've long had an issue with periods of greatly elevated urine flow - such as experienced by diabetics, though I've never been found to show insulin insenitivity. I believe the urination issue (and many other issues I've had) are related to elevated norepinephrine. In the past I tried to get my doctors to look at this more closely and was referred to a psychologist which resulted in prescriptions for anti-anxiety medications I never filled or took. Hopefully now that I have multiple blood tests showing other hormone imbalances such as the elevated testosterone and lack of growth hormone I can get some traction with an endocrinologist and get this properly investigated.

C-reactive protein, <3, <3 3 yrs ago, ref range <5 mg/L
ESR westergren, 4, 3 1 yr ago, ref range 0-25 mm/Hr
These are markers for inflammation. I think these numbers are ok. I believe my low carbohydrate diet ought to be anti-inflammatory and my increased exercise might be increasing it short term, but long term ought to be anti-inflammatory as my fitness improves.  I've started eating some flax and chia both rich in omega 3 fatty acids which should be anti-inflammatory at least with respect to cardiovascular health. I've also begun taking a DHA/EPA supplement Ovega-3 500 mg/day.

glucose ser/plasma 92, ref range 60-109 mg/dL
Higher than I expected given my low carb diet. Maybe this is elevated by high norepinephrine?

chloride 98, ref range 95-108 mmol/L
sodium 141, ref range 134-149 mmol/L
potassium ser/plasma 4.5, ref range 3.5-5.0 mmol/L
anion gap 18, ref range 6-15 mmol/L
I'm glad my potassium level is not too high as I take potassium losartan for blood pressure and eat a lot of potassium rich foods. I think the high anion gap is a calculated value which is due to my chloride being low normal and my sodium being higher. And I think that may be a normal side effect of the diet I'm on.

carbon dioxide 25, ref range 23-30 mmol/L
I think this low normal value is good. Being too low can be a sign of dehydration or liver or kidney damage.

BUN 15, ref range 7-20 mg/dL
creatinine 0.5, ref range 0.5-1.4 mg/dL
glomerular filtration rate estimate, >120, ref range >59 mL/min/BSA
Creatinine is probably low due to having low muscle mass and maybe also due to high urine volume. The high calculated GFR is probably meaningless if the low creatinine level is just due to having little muscle.

calcium, 10.2, ref range 8.4-10.2 mg/dL
High normal is hopefully ok. Too high can indicate excess parathyroid hormone leaching calcium from bones. This would be bad in combination with long term caloric restriction which can accelerate loss of bone density, especially with aging. Could my other hormone abnormalities be related to elevated PTH?

bilrubin total, 0.4, ref range 0.1-1.0 mg/dL

total protein, 8.0, ref range 6.0-8.3 g/dL
High normal hopefully just another indication of mild dehydration?

alk phos serum 32, ref range 30-120 U/L
Low normal hopefully indicates a healthy liver? My vitamin D level was low this winter and I began taking 1000 IU/day and I've been getting more sun with the warmer weather.  Coeliac disease is also listed as a cause of low levels. I don't think I have it, though I do get a coeliac type of response to eating most legumes which I've been increasingly avoiding for the past few years.

AST (SGOT), 66, ref range 8-37 U/L
ALT (SGPT), 53, ref range 8-35 U/L
Probably due to high CK and hopefully not indicative of liver dysfunction. I've been taking vitamin B3 as nicotinamide riboside 250 mg/day and recently added B3 as nicotinic acid 500 mg/day which at higher levels can lead to liver issues.

cholesterol 228, ref range 120-199 mg/dL
HDL cholesterol 58, ref range 40-80 mg/dL
LDL cholesterol 123, ref range 60-129 mg/dL
triglycerides 235, ref range 30-149 mg/dL

They've all been poor for a long time. I had a doctor want to get me started on statins when I was 30 which I refused because the list of side effects was the list of issues I was already experiencing to some degree. I was hoping my low carb fat burning diet would have lead to a bigger improvement. My guess this is due to my hormone imbalances in particular having elevated norepinenphrine.  Nicotinic acid at higher doses is good for reducing cholesterol with increasing risk for liver trouble.

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I'm sorry your blood chemistry didn't improve in some of the ways your were hoping it would as a result of your diet and lifestyle modifications. Given your condition it is really hard to say just what impact CR will eventually have on your biomarkers, or why some of your blood chemistry is/remains so unusual. You are clearly facing a lot of health challenges, but at least you are doing it now from a somewhat better informed position.


Did you get your IGF1 level tested? It is likely to drop with CR, which in your case may not be a good thing, so you should probably monitor it.



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Dean, the IGF1 test wasn't done.  These tests were ordered by my rheumatologist during a visit that was a little rushed and insufficiently long for me to properly convey evereything I was hoping to get done.  I'll follow through on my next visit with my neurologist in about 3 months and try and get it done then.  Any suggestions for other tests likely relevant would be appreciated.


I'm still hopeful the numbers will be improved through diet.  Less than two months dieting isn't much time and the aggressive phase only lasted 3 weeks. 

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I have high LDL and TC (though also low TG and high HDL), so I am always interested in interventions which might lower my TC (primarily through lowering LDL). I have done quite a bit of research on fiber and as one may expect, the picture is complicated. There is no question that a high fiber diet is beneficial (as Dean champions), but the different fiber types achieve their beneficial effects through different mechanisms. Specifically to cholesterol control, it appears that viscosity is the most important characteristic of the fiber:


PMID: 21736815 


Viscosity rather than quantity of dietary fibre predicts cholesterol-lowering effect in healthy individuals.


So it's worth exploring the highest viscosity fiber, such as glucomannan, rather than just the medium (or low) viscosity ones. Controlling through fiber has advantages in this situation, because statins can be hard on muscle tissue and in some scenarios such as heavy muscle exercise, cholesterol may even assist in recovery and muscle repair (I would speculate that perhaps this condition might mimic the same need for muscle recovery even without heavy exercise).


However, it is hard to judge how bad your LDL is - because going by sheer number one might think it's highish but not disastrously so (mine is higher!) - what is key is finding out the true picture of your LDL, where this overall number is not as meaningful, because it depends in large part on the size of your LDL particles (which can be measured) - fewer and larger particles will show as a "bigger" overall LDL number and yet be healthier than more of the particles that are smaller in size which shows up as a smaller LDL number that ends up more unhealthy. In any case, the bigger issue, just going by numbers is your TG. That is what I would concentrate on as a clear negative in your lipid profile. Concentrate on getting that number down, and you'll also find your calculated cholesterol numbers improve.


There is another way of approaching the question of IGF1, TG and cholesterol, perhaps killing three birds with one stone (sorry for the morbid expression). You might try swapping some of your protein sources in favor of getting more of your protein from whey protein isolate. Whey protein generally elevates IGF-1, but interestingly enough can lower your cholesterol and triglycerides, particularly for someone who is or has been recently overweight:


PMID: 20377924


Effects of whey protein isolate on body composition, lipids, insulin and glucose in overweight and obese individuals.


"Fasting TAG levels were significantly lowered in the whey group compared with the control group at 6 weeks (P = 0.025) and 12 weeks (P = 0.035). There was a significant decrease in total cholesterol and LDL cholesterol at week 12 in the whey group compared with the casein (P = 0.026 and 0.045, respectively) and control groups (P < 0.001 and 0.003, respectively). Fasting insulin levels and homeostasis model assessment of insulin resistance scores were also significantly decreased in the whey group compared with the control group (P = 0.049 and P = 0.034, respectively). The present study demonstrated that supplementation with whey proteins improves fasting lipids and insulin levels in overweight and obese individuals."


Sounds like win-win-win to me. Now, of course, this is contrary to the general vegan drift favored around here, but I think if you are consuming animal-sourced protein for health reasons, there should be no ethical qualms. If I were in your situation, I'd also throw in modest amounts of wild-caught salmon and/or sardines, since it's a good source of critical nutrients including marine omega-3 and vitamin B12 - small amounts are OK, no need to overdo it.

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cholesterol 228, ref range 120-199 mg/dL

HDL cholesterol 58, ref range 40-80 mg/dL
LDL cholesterol 123, ref range 60-129 mg/dL
triglycerides 235, ref range 30-149 mg/dL


If you are worried about the cholesterol (as I would be in your situation), why not do both yourself and your chickens a favor and cut out the damn eggs?


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Tom thanks much for the suggestions.  I will look at them carefully.


Dean, both my hdl and ldl used to be outside their reference ranges, hdl low and ldl high.  I got sick eating legumes.  At first I thought it was just chickpeas.  Then I had to give up black beans.  And shortly after I had to stop eating pintos, navy beans, green beans and the cave beans and all the other unusual varieties we were growing. Eventually I got smart and elimanted all peas, lentils and soy.  I stopped making tempeh and tofu and eliminated most anything made from soy and various common food additives such as guar gum.


I believed dietary protein was important to slow muscle loss and I started eating eggs after giving up black beans.  As I gave up more beans I ate more eggs.  We sought out high quality eggs but one day I got fresh eggs from one of my sustainable gardening friends who keeps chickens and I was blown away by how fabulous they were compared to the expensive organic, free range, vegetarian fed, humane, blah, blah, blah eggs I had been buying at the local farmer's market.  Which prompted us to add chickens to our gardening.


My cholesterol numbers have been improving, hdl rising and ldl dropping.  I don't know if it is losing the beans or adding the eggs or something else but I have no reason to think the eggs are causing me harm and I don't know of any other foods that provide as good a mix of amino acids with such low carbohydrate content and low total calories.  And to stop consuming eggs would be of zero benefit to the chickens and would only reduce my incentive to provide them with a good diet.


My triglycerides have jumped upwards.  They used to be high but tended towards a little above or a little below the high end of the reference range and there wasn't a noticeable change as I ate more eggs.  I'm guessing the jump in triglycerides is due to my high norepinephrine.  I previously had trouble with my blood glucose spiking and crashing after stress which lead me to consuming lots of orange juice and other concentrated sugars.  And perhaps with the elimination of high glycemic carbs my high norepinephrine is having a greater impact on triglycerides.  I was expecting the diet would have lowered triglycerides instead of raising them, but perhaps an endocrinologist will be able to help me sort this out.  For the short term the rise in triglycerides has prompted me to begin taking nicotinic acid which is supposed to counter norepinephrine induced mobilization of FFAs.

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Just now, reading online about blood testing for lipids and glucose, in addition to fasting (which is included in the instructions provided by my doctor/hospital) one is also supposed to avoid exercise.  I rode my bicycle to the hospital almost 8 miles with a headwind.  The nearest bicycle rack was a block away and it was a very long for me walk to and through the building.  The wind slowed me down and I pushed hard on the verge of collapse for much of the ride and the subsequent walk.  The blood was drawn less than an hour after my arrival.  That probably somewhat invalidates the results and to some degree most previous ones as well.

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  • 4 weeks later...

New paper helps to explain why my dietary changes have had such a profoundly beneficial effect.  Dean, I'd love to hear your interpretation of this paper as you have such insight into metabolic issues.  My final impression is that while being CR'd and in ketosis has proven excellent for me I probably should stop the CR before I get too thin by boosting my fat intake, perhaps to levels that make normal people diabetic.


I had been planning to drop to the low end of the BMI range, 18.5-19.5 thinking that with my low muscle mass that would be a good target.  I'm currently at 155 lbs (5'10") and am fairly certain it is ok to drop a few more pounds but will have to rethink shedding all of my pinchable body fat.


It looks like my hyperlipidemia may be a protective response to neuromuscular disease and is correlated with longer survival in ALS.



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After reading this paper again in which they establish that a high fat diet doubles the life span of SBMA knock-in mice, I think it might also offer insights to numerous other issue discussed here regarding sarcopenia and the benefits of higher body fat in older age, as well as the induction of insulin resistance / metabolic syndrome when body fat percentage is very low.

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I read the paper on SBMA and a high fat diet you pointed to. That is one interesting disease you've got there...


I won't pretend to have groked the study in it's entirety, but here is the understanding I came away with.


It appears that SBMA results in a shift in major skeletal muscles (like quadriceps and gastrocnemius muscles) from predominantly fast-twitch, anaerobic, glucose-metabolizing (glycolytic) muscle fibers to slow-twitch, aerobic, lipid-metabolizing, mitochondria-rich, oxidative muscle fibers. 


One might not normally think of this shift as such a bad thing. It might be expected to make someone a better endurance athlete, rather than a sprinter. But somewhere along the way, something goes horribly wrong in those with SBMA, and muscle cells end up dying, and muscles atrophying. 


Here is the pathway I think they are suggestion based on the evidence from the SBMA knock-in mice they studied:


Testosterone binds to messed up AR in fast-twitch muscles → ↑ mTOR activity → ↑ PGC1α → ↑ (dysfunctional) mitochondria synthesis → ↑ oxidative metabolism → ↑ oxidative stress → ↑ muscle cell autophagy → muscle wasting


In words, when testosterone binds to an SBMA sufferer's messed up androgen receptors in big, fast-twitch-dominated muscles, it increases activity of the anabolic regulator complex we all know as mTOR. mTOR in turns churns out PGC1α, which promotes mitochondrial biosythesis. With more mitochondria in muscle cells, the muscles cells turn from inefficiently metabolizing glucose for ATP to using mitochondria-orchestrated oxidative phosphorylation (oxphos) to make ATP, and in the process convert from being mostly glycolytic fibers to mostly oxidative fibers. They also end up metabolizing more lipids, and less glucose.


But unfortunately it appears the new muscle mitochondria are messed up for some reason unknown to the authors, with their membranes significantly depolarized. They suggest that these dysfunctional mitochondria may generate free radicals (ROSs), which cause oxidative damage. This in turn induces mTOR to express autophagy-promoting genes, inducing muscles cell autophagy, causing the muscles cells to die and therefore the muscles of SBMA sufferers to atrophy.


What they found in muscles of SBMA knock-in mice is that a high fat diet (HFD) blocked the increase in mTOR and PGC1α, preventing (or at least attenuating) the switch from fast-twitch, glycolytic metabolism to slow-twitch, oxidative metabolism in the major skeletal muscle, reducing autophagy and muscle wasting. 


When the SBMA knock-in mice were fed the HFD, they were better able increase their weight and maintain lean muscle mass (i.e. much less wasting) and actually increased their fat deposits. But unlike normal mice fed a HFD, the SBMA mice didn't become obese, and didn't develop glucose intolerance or insulin resistance, despite eating the same amount and being no more physically active than control mice fed the HFD. And best of all, the SBMA mice lived longer when fed the HFD compared with SBMA mice fed normal chow. 


This positive metabolic response to a HFD in SBMA mice (i.e. eating lots of calories from a high fat diet, increasing adipose tissue and preserving lean muscle mass while maintaining good glucose metabolism), reminds me of the response elicited by cold exposure, and in particular an increase in brown / beige fat. The authors hint at that possibility in the last couple paragraphs of the paper, saying:


Our results provide proof-of-principle that an HFD ameliorates
muscle pathology, improves motor function, and
extends life span of a mouse model of SBMA. The HFD
ameliorated SBMA mouse phenotype by possibly affecting
several tissues and metabolic pathways. In addition to muscle,
the effect of diet may also come from adipose tissue. AR [Androgen receptor]
is highly expressed in adipose tissue, and the effect of polyglutamine
expansion in AR [the genetic mutation SBMA folks have - DP] on
this peripheral tissue remains to be addressed. Our findings suggest
an unprecedented role for adipose tissue in SBMA.


I tried doing a search for SBMA and brown fat or thermogenesis and couldn't find anything.


But regardless of whether or not brown/beige fat is involved in the improvements the SBMA mice enjoy as a result of a high fat diet, the important thing this paper shows is a pretty dramatic benefit from eating a HFD.


Given these results, if I were you Todd I'd seriously consider eating a high fat diet, although given your uneviable serum cholesterol profile, I'd make sure it is a diet high in healthy fats.


I also question your (prior?) plan to drop your weight dramatically to a BMI of 18.5 - 19.5. Heck, I don't think this is wise for completely healthy folks, especially as our age creeps up, due to concern about sarcopenia (not to mention other things like bone health and immunocompetence). It boggles my mind to think you'd be considering dropping that much weight, given your genetic proclivity (or viewed pessimistically, your destiny) for pathological muscle wasting.


Instead, I'd opt for a super-healthy, calorie-replete, high-fat diet in order to maintain my weight and muscle mass. What type and how much exercise someone with SBMA should engage in is a tough call. Despite the fact that it's a muscle wasting disease, exercise does not appear to provide much benefit for people with SBMA (see here, here and here). This study might suggest why - namely that exercise (esp aerobic exercise) could boost muscle mitochondria biosynthesis and promote the shift towards oxidative metabolism. Given the messed up mitochondria that result, this increased mitochondrial activity to support the metabolic load of exercise could paradoxically accelerate muscle wasting via autophagy rather than preserve muscle mass. In short, you may be in the uneviable position of "use it and lose it" when it comes to muscles, and hence damned if you do (exercise) and damned if you don't (exercise).


Here is hoping that researchers will come up with an effective SBMA treatment soon.  Perhaps SBMA needs the equivalent of the Ice Bucket Challenge, which appears to have fostered a big breakthrough towards understanding and treating that other degenerative disorder, ALS.



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Dean, thanks for your interpretation.  The study suggests that a HFD begun early is protective.  But I wasn't sure if the same mechanism is still beneficial when started later, after there has been a major shift from glycolytic to oxidative muscle fibers and major atrophy?  This excerpt from the article suggests to me a late shift to a HFD is beneficial:  "while the HFD did not affect mitochondrial complex activity, it decreased mitochondrial membrane depolarization induced by oligomycin, indicating that the HFD improves mitochondrial quality control."  Also I wonder if part of the mitochondrial problem could be related to a NAD+ deficit.  SIRT1 mediated deacetylization consumes NAD and is likely up regulated in SBMA.  Lately,I've been taking nicotinic acid at 1000 mg/daily + 250 mg/daily of nicotinamide riboside.   When I began NR there was no obvious effect, but I perceived gains in performance when I added NA at 500 mg/daily and when I increased it to 1000 mg.  One day I skipped both NA and NR and felt increasingly sluggish by evening where I had losses of roughly both 1/3 in speed and distance of my evening walk.  I need more testing to be highly confident of these results but so far it is suggestive of importance.

Another recent paper might indicate an alternative reason why my new diet has been good so far.
It suggests a major source of impairment is loss of synaptic drive and hypothesizes one factor may be a deficit of BDNF found in SBMA muscle.  From what I've read elsewhere, a low carb diet with exercise ought to be boosting BDNF.


As for the question of should I continue weight loss, at my current weight of 155 lbs I still have a LOT of fat.  Before I started this diet and exercise regimen I didn't realize just how fat I was.  I thought of myself as doughy without perception of where fat ended and muscle began.  But now I'm keenly aware of how little muscle and how much fat I have.  Because of the amount of muscle I've lost at a given BMI my body fat percentage is going to be much higher than average.  I wish there were good biomarkers for me to track to inform the decision to continue weight loss, but for the moment I'm inclined to follow the imprecise results of my performance at exercise.  Hopefully as long as my performance is increasing then weight loss is not resulting in significant loss of muscle.  Here's a paper that suggests high protein intake, particularly leucine and animal sources such as milk & red meat may counter muscle loss while CR'd, DOI: 10.1186/1743-7075-9-83  On the other hand because this involves up regulating mTOR perhaps it just aggravates the problem with bad mitochondria?

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All good questions, for which there are no definitive answers. It is hard enough to know what's best for regular folks. In your very special case, it's virtually impossible since stuff that might work to improve health and longevity in regular people may be detrimental for you, given your condition. Unfortunately, that means you are pretty much on your own, flying blind by the seat of your pants. 


It seems like monitoring your creatine kinase (CK) level on a regular basis (which I know you do) in order to track ongoing muscle damage associated with  exercise and CR is worthwhile. Much less accurately, but perhaps worthwhile nonetheless, do you have or have you considered a scale that assesses body composition? They provide nowhere near as accurate data on lean and fast mass as as a DEXA scan, but I've found mine to provide consistent and repeatable data that allows me to track changes in body composition over time.



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Dean, by body compostion scale do you mean the inexpensive ones that apparently measure electrical resistance through your feet?  I had read they are wildly inaccurate as they are affected by the moistness of your skin, your hydration level, the temperature and other factors that can overwhelm the difference in electrical conductivity of muscle and fat.  Maybe with your consistent regimen you minimize the factors generating noise leading to a good result?  If so, perhaps I can do the same.  Those scale are cheap enough that even if it didn't work well for me it would be no big deal.  My scale has a problem that the reading varies by up to 1.5 lbs as I shift my weight forward or back.  I've learned to mostly compensate for that and maybe the quirks of a body composition scale are also learnable.

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Yes, I'm talking about the bioimpedence scales that you are thinking of. Regarding accuracy - I don't claim they are accurate. But I find (at least mine) to be extremely repeatable day-to-day, as long as I weight myself without wet feet, immediately after I get up in the morning so with consistent (de)hydration. I'll admit they are far from perfect, but I've found my bodyfat scale to be pretty useful. They aren't very expensive. I'd consider it if I were you, since losing muscle mass while dropping weight is obviously a much bigger deal for you than most people.



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