Fascinating stuff!
I am learning so much. Love it.
Fidel's tests
Re: Fidel's tests
I remember reading that paper too. It made me wonder about the hormesis theory. Maybe E4s thrive in adversity; very hot or very cold weather?I found a 2010 paper (Eisenberg et al.) that suggests a benefit of E4 in hotter or colder climates (the apoE latitude hypothesis), but less so in moderate climates, which would explain the data to some extent.
Fidel, I'd be careful drawing any dietary conclusions from that old Moreno paper. There are only eight 3/4s and zero 4/4s in the data sample. A careful reading of Table 5, however, reveals that E4 carriers actually demonstrated the LOWEST TC, LDL-C, and apoB on a higher MUFA diet; while still maintaining a decent HDL-C/apoA-1 level. If anything, the data supports the use of MUFAs for E4s.
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Gilgamesh
- Contributor
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- Joined: Sat Oct 26, 2013 11:31 am
- Location: Northeast US mostly
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Re: Fidel's tests
That's exactly how I look at it. I frame the answer to the question about global APOE allele distribution like so: APOE-ε4 stinks, for everyone. There are people for whom it stinks a bit less: people at risk of two types of nutrient shortage -- those at risk for a vitamin D shortage (those living far away from the equator), and those at risk for the many other types of nutrient shortages (including cholesterol -- or nutrients that help us maintain cholesterol levels) associated with dysentery and other diseases causing the runs (mostly, on average, people living closer to the equator).Juliegee wrote:Maybe E4s thrive in adversity; very hot or very cold weather?
Recent (evolutionarily) Iberian immigration to Latin America makes this area the one major exception to allele distribution.
Will look up the Eisenberg paper.
Un abrazo
GB
Re: Fidel's tests
Thank you for taking the time to dig into that study more deeply. You're right, on most parameters MUFA had a beneficial effect for the 3/4 test group.Juliegee wrote:
Fidel, I'd be careful drawing any dietary conclusions from that old Moreno paper. There are only eight 3/4s and zero 4/4s in the data sample. A careful reading of Table 5, however, reveals that E4 carriers actually demonstrated the LOWEST TC, LDL-C, and apoB on a higher MUFA diet; while still maintaining a decent HDL-C/apoA-1 level. If anything, the data supports the use of MUFAs for E4s.
3/4
20% fat for a month
Got the best blood test results i’ve seen for myself at the 6.25 year mark into totally plant-based eating. The standard test showed these numbers:
total cholesterol = 144, triglycerides = 79, HDLc = 41, LDLc = 87, non-HDLc = 103
while the advanced Cardio IQ panel for the same showed:
total cholesterol = 123, triglycerides = 73, HDLc = 35, LDLc = 73, non-HDLc = 88
The differences in the two testing methods is noteworthy in itself. The latter test shows me actually too low for total cholesterol (according to the Quest Lab), as well as for HDLc, but i’m reading the overall result as positive, placing me in what some call a “heart attack proof” range, at least in terms of heart attacks resulting from atherosclerosis. The main thing i attribute the results to is lower body weight, a body mass index of 17.3 at the time of the test, a level considered underweight but maybe it isn’t if nutrient requirements are being met. Though the diet i was on could be perceived as calorie-restricted, it could also be seen as healthy since i was getting all needed nutrients. It was sort of a plant-based version of the CRON diet (calorie restricted optimal nutrition) at http://gg.gg/CRON-diet. Was using cronometer.com to keep track of how i was doing.
I got to the lower body weight with a grain-free month before bringing quite a bit of grains back in, most of it whole, much of it sprouted. Foods i was regularly eating included oat bran, bananas, almond meal, freshly sprouted grains, sprouted grain bread, whole wheat pasta, curry spices, commercial mock meats, daiya cheese alternatives, mindful mayo, soy protein isolate, chia seeds, brazil nut (¼ nut daily), grapefruit peel, ascorbic acid powder. Allowed a half ounce of spinach a day to help meet vitamin K needs.
Won’t continue daily consumption of soy isolate after considering tests showing aluminum in it, like the one Dr. Harris ordered: http://gg.gg/soy-AL
Was eating a mostly low sulfur diet, except for the soy powder & mock meats. Added calcium carbonate powder to recipes, since it’s hard to find a low sulfur plant-based source of calcium.
The macronutrient ratio i was at was about 60% carbohydrates, 20% fat (under 6% saturated), 20% protein. Was doing that to test a recommendation for the apoE gene variant i have, suggested by perfectgenediet.com Have since gone back to closer to 10% protein, thinking that higher protein was giving me too much of a sulfur load. Received a homocysteine reading of 11.5 umol/L which is not considered high by the test lab, but it probably would have been lower if i hadn’t been eating that much protein, as homocysteine is biosynthesized from the sulfur-containing amino acid methionine found in protein.
The 20% fat advice does seem to work alright for me, for the most part, as i got what is considered improvements in lipoprotein particle sizes, a 31 point drop in small LDL, a 431 point increase in large HDL. This contradicts blanket statements on pro-paleo websites that eating less fat will increase small LDL and decrease large HDL. While eating 20% fat for a month resulted in improvements, it did not move particle sizes out of the high risk range. I wonder if eating that way for a year or more would do so.
LDL particle number remained in optimal range at 1145 nmol/L.
Did see a worsening of Lp(a) from optimal to a moderate risk level of 83 nmol/L.
The large drop in triglycerides from 120 on the last test to the 70’s on this one i attribute partly to a reduction in refined carbohydrates from daily to once weekly. Was able to get all the good numbers while still eating things like sugary vegan ice cream and saturated-fat-laden vegan cheezecake once a week. If you do something once a week, rather than every day, that’s an 86% difference. Did i get the math right on that? Anyway, it was enough to get fasting glucose back from a high reading of 102 to 90. Continuing a grazing eating pattern probably helped that occur as well, guarding against too much of a glycemic load at any one meal.
The grazing eating pattern strikes me as better for digestion as well, giving my body the upper hand on food, not overwhelmed with too much at once, helping to ensure the presence of enough digestive enzymes for a given meal. It also decreases the tendency to get bored with food, keeping me interested in eating. Even though i was eating only a couple hundred calories or so when i ate, i didn’t feel deprived because no more than a couple hours would go by before stimulating my taste buds again. It wasn’t a struggle.
The study http://gg.gg/eating-freq shows higher eating frequency among those who maintain weight loss.
My total white blood cell count always comes in low, this time at 3.29 x10(3)/uL. If i view a white blood cell count as an inflammatory marker, perhaps that could be seen as a positive?
Vitamin D3 level came in at 49 pg/mL which is good.
Magnesium level showed as 2 mg/dL which is normal. Wasn’t supplementing magnesium, although i have at times since i have magnesium chloride crystals which i got to make nigari tofu but never did, so i’ve added it to other recipes to make use of it.
All of the ion mobility fractionation numbers are as follows:
LDL particle number = 1145 nmol/L (optimal)
LDL small = 229 nmol/L (high risk)
LDL medium 219 nmol/L (moderate risk)
HDL large = 4742 nmol/L (high risk)
LDL pattern = B (high risk)
LDL peak size = 215 angstrom (high risk)
ApoB = 93 mg/dL (moderate risk)
total cholesterol = 144, triglycerides = 79, HDLc = 41, LDLc = 87, non-HDLc = 103
while the advanced Cardio IQ panel for the same showed:
total cholesterol = 123, triglycerides = 73, HDLc = 35, LDLc = 73, non-HDLc = 88
The differences in the two testing methods is noteworthy in itself. The latter test shows me actually too low for total cholesterol (according to the Quest Lab), as well as for HDLc, but i’m reading the overall result as positive, placing me in what some call a “heart attack proof” range, at least in terms of heart attacks resulting from atherosclerosis. The main thing i attribute the results to is lower body weight, a body mass index of 17.3 at the time of the test, a level considered underweight but maybe it isn’t if nutrient requirements are being met. Though the diet i was on could be perceived as calorie-restricted, it could also be seen as healthy since i was getting all needed nutrients. It was sort of a plant-based version of the CRON diet (calorie restricted optimal nutrition) at http://gg.gg/CRON-diet. Was using cronometer.com to keep track of how i was doing.
I got to the lower body weight with a grain-free month before bringing quite a bit of grains back in, most of it whole, much of it sprouted. Foods i was regularly eating included oat bran, bananas, almond meal, freshly sprouted grains, sprouted grain bread, whole wheat pasta, curry spices, commercial mock meats, daiya cheese alternatives, mindful mayo, soy protein isolate, chia seeds, brazil nut (¼ nut daily), grapefruit peel, ascorbic acid powder. Allowed a half ounce of spinach a day to help meet vitamin K needs.
Won’t continue daily consumption of soy isolate after considering tests showing aluminum in it, like the one Dr. Harris ordered: http://gg.gg/soy-AL
Was eating a mostly low sulfur diet, except for the soy powder & mock meats. Added calcium carbonate powder to recipes, since it’s hard to find a low sulfur plant-based source of calcium.
The macronutrient ratio i was at was about 60% carbohydrates, 20% fat (under 6% saturated), 20% protein. Was doing that to test a recommendation for the apoE gene variant i have, suggested by perfectgenediet.com Have since gone back to closer to 10% protein, thinking that higher protein was giving me too much of a sulfur load. Received a homocysteine reading of 11.5 umol/L which is not considered high by the test lab, but it probably would have been lower if i hadn’t been eating that much protein, as homocysteine is biosynthesized from the sulfur-containing amino acid methionine found in protein.
The 20% fat advice does seem to work alright for me, for the most part, as i got what is considered improvements in lipoprotein particle sizes, a 31 point drop in small LDL, a 431 point increase in large HDL. This contradicts blanket statements on pro-paleo websites that eating less fat will increase small LDL and decrease large HDL. While eating 20% fat for a month resulted in improvements, it did not move particle sizes out of the high risk range. I wonder if eating that way for a year or more would do so.
LDL particle number remained in optimal range at 1145 nmol/L.
Did see a worsening of Lp(a) from optimal to a moderate risk level of 83 nmol/L.
The large drop in triglycerides from 120 on the last test to the 70’s on this one i attribute partly to a reduction in refined carbohydrates from daily to once weekly. Was able to get all the good numbers while still eating things like sugary vegan ice cream and saturated-fat-laden vegan cheezecake once a week. If you do something once a week, rather than every day, that’s an 86% difference. Did i get the math right on that? Anyway, it was enough to get fasting glucose back from a high reading of 102 to 90. Continuing a grazing eating pattern probably helped that occur as well, guarding against too much of a glycemic load at any one meal.
The grazing eating pattern strikes me as better for digestion as well, giving my body the upper hand on food, not overwhelmed with too much at once, helping to ensure the presence of enough digestive enzymes for a given meal. It also decreases the tendency to get bored with food, keeping me interested in eating. Even though i was eating only a couple hundred calories or so when i ate, i didn’t feel deprived because no more than a couple hours would go by before stimulating my taste buds again. It wasn’t a struggle.
The study http://gg.gg/eating-freq shows higher eating frequency among those who maintain weight loss.
My total white blood cell count always comes in low, this time at 3.29 x10(3)/uL. If i view a white blood cell count as an inflammatory marker, perhaps that could be seen as a positive?
Vitamin D3 level came in at 49 pg/mL which is good.
Magnesium level showed as 2 mg/dL which is normal. Wasn’t supplementing magnesium, although i have at times since i have magnesium chloride crystals which i got to make nigari tofu but never did, so i’ve added it to other recipes to make use of it.
All of the ion mobility fractionation numbers are as follows:
LDL particle number = 1145 nmol/L (optimal)
LDL small = 229 nmol/L (high risk)
LDL medium 219 nmol/L (moderate risk)
HDL large = 4742 nmol/L (high risk)
LDL pattern = B (high risk)
LDL peak size = 215 angstrom (high risk)
ApoB = 93 mg/dL (moderate risk)
Last edited by Fidel on Mon Jul 27, 2015 7:57 pm, edited 1 time in total.
3/4
Re: Fidel's tests
Wow, Fidel- another jam-packed post 
Congrats on the continued terrific LDL-P! For ease of comparison, I put your two tests side by side, excluding the standard lipids as the advanced information basically overrides them.
For both tests you reported eating a plant based diet. For the June test: 60% carbs, 30% fat (7% saturated), 10% protein. For the July test: 60% carbs, 20% fat (under 6% saturated), 20% protein.
June Test/July Test
LDL-P: 1139,1145 (optimal)
ApoB: 91/93 (moderate risk)
Small LDL: 260, 229 (high risk)
Medium LDL: 215, 219 (moderate risk)
LDL Peak size: 210.3, 215 (high risk)
LDL Pattern: B, B (high risk)
Large HDL: 4311, 4742
Glucose: 102, 90
A1c: 5.5, ?
Homocysteine: ?, 11.5
Lp(a) 72 nmol/L (optimal), 83nmol/L (moderate risk)
I noted those improvements with interest. Did exercise change between the two tests? What about alcohol consumption? I wonder if you could attribute those improvements to this:
Your BMI is pretty low. You’re certainly catabolizing some muscle. Are you strength training to counteract that? We also have evidence that sarcopenia drives neurodegeneration which begins decades before the first symptom manifests. How do you overall feel; strong/energetic or weak/tired? (I’ve noticed I tread a fine line with CRON.) I feel great with my BMI around 18.5. When I drop much lower, I feel under-powered.) It's hard to exercise if you're feeling puny. Exercise seems to be the strategy with the MOST evidence to prevent neurodegeneration for E4 carriers.
Are you concerned with your Lp(a) rise or your “at-risk” particle sizes? I’m aware of Peter Attia’s stance, but what if he’s wrong? (I'm scared enough to heed BOTH number and size.) Research also suggests that HDL may be vitally important for E4 carriers; helping with both reverse cholesterol transport and amyloid clearance. Yours is really low. I wonder if you could substitute some of your carbs for a little more plant-based MUFA to address all of these issues?
I greatly appreciate your sharing, my friend. We earn a lot from diet/lipid shares- THANKS.
Congrats on the continued terrific LDL-P! For ease of comparison, I put your two tests side by side, excluding the standard lipids as the advanced information basically overrides them. For both tests you reported eating a plant based diet. For the June test: 60% carbs, 30% fat (7% saturated), 10% protein. For the July test: 60% carbs, 20% fat (under 6% saturated), 20% protein.
June Test/July Test
LDL-P: 1139,1145 (optimal)
ApoB: 91/93 (moderate risk)
Small LDL: 260, 229 (high risk)
Medium LDL: 215, 219 (moderate risk)
LDL Peak size: 210.3, 215 (high risk)
LDL Pattern: B, B (high risk)
Large HDL: 4311, 4742
Glucose: 102, 90
A1c: 5.5, ?
Homocysteine: ?, 11.5
Lp(a) 72 nmol/L (optimal), 83nmol/L (moderate risk)
I agree with your assessment that higher protein may have had this effect. Have you ever tried supplementing with glycine to counteract that? Have you ever run your methylation snips to see if you have any underlying issues? What is your current supplementation schedule for B vitamins? FWIW, as an E4 carrier, 11.5 mol/L is too high. Most of us are shooting for numbers <9 to help prevent AD and CAD.Received a homocysteine reading of 11.5 umol/L which is not considered high by the test lab, but it probably would have been lower if i hadn’t been eating that much protein, as homocysteine is biosynthesized from the sulfur-containing amino acid methionine found in protein.
I, and others here, have dealt with the same low WBC levels. I agree; could be positive…My total white blood cell count always comes in low, this time at 3.29 x10(3)/uL. If i view a white blood cell count as an inflammatory marker, perhaps that could be seen as a positive?
FWIW, lipidologists also suggest that eating less fat will increase small LDL-P and decrease large HDLThe 20% fat advice does seem to work alright for me, for the most part, as i got what is considered improvements in lipoprotein particle sizes, a 31 point drop in small LDL, a 431 point increase in large HDL. This contradicts blanket statements on pro-paleo websites that eating less fat will increase small LDL and decrease large HDL.
I noted those improvements with interest. Did exercise change between the two tests? What about alcohol consumption? I wonder if you could attribute those improvements to this:
Congrats on the fasting glucose drop from 102 to 90. It would be great to reduce that even more. Do you ever check post-prandial glucose? Did you check A1c this time? Have you checked fasting insulin yet? I worry that grazing will elevate that number rendering you more susceptible to IR. Apologies for so many questions, but remind us again of your age. I ask as IR tends to become more of an issue as we get older.The large drop in triglycerides from 120 on the last test to the 70’s on this one i attribute partly to a reduction in refined carbohydrates from daily to once weekly.
Your BMI is pretty low. You’re certainly catabolizing some muscle. Are you strength training to counteract that? We also have evidence that sarcopenia drives neurodegeneration which begins decades before the first symptom manifests. How do you overall feel; strong/energetic or weak/tired? (I’ve noticed I tread a fine line with CRON.) I feel great with my BMI around 18.5. When I drop much lower, I feel under-powered.) It's hard to exercise if you're feeling puny. Exercise seems to be the strategy with the MOST evidence to prevent neurodegeneration for E4 carriers.
Are you concerned with your Lp(a) rise or your “at-risk” particle sizes? I’m aware of Peter Attia’s stance, but what if he’s wrong? (I'm scared enough to heed BOTH number and size.) Research also suggests that HDL may be vitally important for E4 carriers; helping with both reverse cholesterol transport and amyloid clearance. Yours is really low. I wonder if you could substitute some of your carbs for a little more plant-based MUFA to address all of these issues?
I greatly appreciate your sharing, my friend. We earn a lot from diet/lipid shares- THANKS.
July tests
Hi, Julie. The first of the 2 tests is really an April test followed by the July test. A grain-free month came right after the April test, then another month, then a lower fat & higher protein month before the early July test. So i’m fixing the comparison you typed, adding other parameters and noting changes i personally consider at least somewhat significant:
April Test/July Test
LDL-P: 1139,1145 (optimal)
ApoB: 91/93 (moderate risk)
Small LDL: 260, 229 (high risk) improvement
Medium LDL: 215, 219 (moderate risk)
LDL Peak size: 210.3, 215 (high risk) improvement
LDL Pattern: B, B (high risk)
Large HDL: 4311, 4742 improvement
Glucose: 102, 90 improvement
A1c: 5.5, 5.5
Homocysteine: ?, 11.5
Lp(a): 72 nmol/L (optimal), 83 nmol/L (moderate risk) worsening
cholesterol: 173, 123 improvement
TG: 120, 73 improvement
LDLc: 107, 73 improvement
HDLc: 42, 35 worsening
cholesterol/HDLc: 4.1, 3.5 improvement
TG/HDLc: 2.8, 2.1 improvement
non-HDL cholesterol: 131, 88 improvement
Agree that a lower number would be better for homocysteine. Suspect i had a single digit number there before testing 20% protein, something which was messing up my low sulfur diet. In the vegan community, we hear quite a bit about how meat eaters eat too much methionine, but it appears plant protein can deliver too much of it as well, when eaten in excess.
Have never tried supplementing with glycine, nor have i ever run methylation snips.
B12 is the only B i’m supplementing, presently at only 1000 mcg of liquid sublingual methylcobalamin once weekly, since i came in too high for B12 the last time it was tested. Less dietary protein is likely enough to get a better homocysteine number, and perhaps a bit more food-borne folate.
It’s interesting that cysteine is one of the two amino acids which is involved in distinguishing one apoE type from another. ApoE 4-4 folks have no cysteine in positions 112 & 158 of apolipoprotein E, while apoE 3-4 people like me have one cysteine in the 4 varying positions, and apoE 2-2 people have cysteine in all 4 positions. Did i get that right?
Read that apoE4 people are not as good at clearing fat and toxins from their systems, compared to apoE2 people. Also read that sulfur is important to detoxification, so maybe cysteine (which contains sulfur) is playing a role in one’s ability to detox. Or it could simply be that a lower ability to clear fat associates with a lower ability to clear toxins since toxins have affinity for fat.
Exercise was about the same between the 2 tests, a bit of daily walking and a leisure bike ride every few days or so.
Alcohol consumption remained the same at zero.
The improvement in lipoprotein particle sizes could very well be due to the lower triglyceride level which itself was likely due to less refined carbs.
Did a bunch of postprandial glucose tests a while back. Haven’t in some time. A1c remained at 5.5. Asked for a fasting insulin test but was turned down, as the physician didn’t find it necessary. I don’t find it critical either at this point. I suppose i could ask a naturopath to get that for me, should i decide i want that at some point.
My age is 54.
Am not strength training. My energy level is pretty good, especially considering my situation. What i mean is i’m doing caregiving in which i’m repeatedly abruptly woken from sound sleeps, something which is far from the healthiest situation, as my natural biorhythm is messed with too much. If it wasn’t for that, i sense i’d be fine continuing with the same diet, but while i’m doing this type of caregiving, i could probably use more long term fuel from more dietary fat, so i might head in that direction for now. Maybe i could test a year or more at 20% fat later on when i have a situation better suited to it.
More dietary fat could help get my HDLc up to a better level, and maybe even get that Lp(a) back to optimal. With LDLc & LDLp as low as i have it now, i might not need that much HDL for reverse cholesterol transport, but like you said, it could have other beneficial functions.
The particle sizes don’t freak me out, as long as i can maintain an otherwise overall positive profile.
Many thanks for your thoughts.
April Test/July Test
LDL-P: 1139,1145 (optimal)
ApoB: 91/93 (moderate risk)
Small LDL: 260, 229 (high risk) improvement
Medium LDL: 215, 219 (moderate risk)
LDL Peak size: 210.3, 215 (high risk) improvement
LDL Pattern: B, B (high risk)
Large HDL: 4311, 4742 improvement
Glucose: 102, 90 improvement
A1c: 5.5, 5.5
Homocysteine: ?, 11.5
Lp(a): 72 nmol/L (optimal), 83 nmol/L (moderate risk) worsening
cholesterol: 173, 123 improvement
TG: 120, 73 improvement
LDLc: 107, 73 improvement
HDLc: 42, 35 worsening
cholesterol/HDLc: 4.1, 3.5 improvement
TG/HDLc: 2.8, 2.1 improvement
non-HDL cholesterol: 131, 88 improvement
Agree that a lower number would be better for homocysteine. Suspect i had a single digit number there before testing 20% protein, something which was messing up my low sulfur diet. In the vegan community, we hear quite a bit about how meat eaters eat too much methionine, but it appears plant protein can deliver too much of it as well, when eaten in excess.
Have never tried supplementing with glycine, nor have i ever run methylation snips.
B12 is the only B i’m supplementing, presently at only 1000 mcg of liquid sublingual methylcobalamin once weekly, since i came in too high for B12 the last time it was tested. Less dietary protein is likely enough to get a better homocysteine number, and perhaps a bit more food-borne folate.
It’s interesting that cysteine is one of the two amino acids which is involved in distinguishing one apoE type from another. ApoE 4-4 folks have no cysteine in positions 112 & 158 of apolipoprotein E, while apoE 3-4 people like me have one cysteine in the 4 varying positions, and apoE 2-2 people have cysteine in all 4 positions. Did i get that right?
Read that apoE4 people are not as good at clearing fat and toxins from their systems, compared to apoE2 people. Also read that sulfur is important to detoxification, so maybe cysteine (which contains sulfur) is playing a role in one’s ability to detox. Or it could simply be that a lower ability to clear fat associates with a lower ability to clear toxins since toxins have affinity for fat.
Exercise was about the same between the 2 tests, a bit of daily walking and a leisure bike ride every few days or so.
Alcohol consumption remained the same at zero.
The improvement in lipoprotein particle sizes could very well be due to the lower triglyceride level which itself was likely due to less refined carbs.
Did a bunch of postprandial glucose tests a while back. Haven’t in some time. A1c remained at 5.5. Asked for a fasting insulin test but was turned down, as the physician didn’t find it necessary. I don’t find it critical either at this point. I suppose i could ask a naturopath to get that for me, should i decide i want that at some point.
My age is 54.
Am not strength training. My energy level is pretty good, especially considering my situation. What i mean is i’m doing caregiving in which i’m repeatedly abruptly woken from sound sleeps, something which is far from the healthiest situation, as my natural biorhythm is messed with too much. If it wasn’t for that, i sense i’d be fine continuing with the same diet, but while i’m doing this type of caregiving, i could probably use more long term fuel from more dietary fat, so i might head in that direction for now. Maybe i could test a year or more at 20% fat later on when i have a situation better suited to it.
More dietary fat could help get my HDLc up to a better level, and maybe even get that Lp(a) back to optimal. With LDLc & LDLp as low as i have it now, i might not need that much HDL for reverse cholesterol transport, but like you said, it could have other beneficial functions.
The particle sizes don’t freak me out, as long as i can maintain an otherwise overall positive profile.
Many thanks for your thoughts.
3/4
-
Gilgamesh
- Contributor
- Posts: 1711
- Joined: Sat Oct 26, 2013 11:31 am
- Location: Northeast US mostly
- Contact:
Re: Fidel's tests
The criteria for underweight are based on correlations with only minimal correction for things that cause both mortality/morbidity and weight loss (cigarette smoking, wasting diseases of all kinds, etc.). There are so many things cause weight loss and worse health that researchers can't control for all of them. I know plenty of people in the CR community with BMIs well below 17 who are doing great.Fidel wrote: The main thing i attribute the results to is lower body weight, a body mass index of 17.3 at the time of the test, a level considered underweight but maybe it isn't if nutrient requirements are being met.
Julie mentioned sarcopenia. This is definitely a concern, but the correlation with neurological problems is just that: a correlation. We really don't know what's causing what. Studies with lab animals show that extreme CR leads to neuroprotection, even when lean muscle mass is lower than in control animals.
People tell me I should be cautious letting my BMI get below 18.5. I tell them they should be cautious letting their BMI get above 18.5. (And we're both probably right! Caution is the watchword.)
(As it turns out, I may have health problems that make extreme CR a bad idea for me, so I'm slowly moving off it. So far, I feel the same or maybe a bit worse, but I'm going to give it time.)
Your diet, by the way, is almost exactly what I ate for years. My current health problems correlate with a move towards higher fat, though I have no idea where the causality lies. I suspect it has little to do with diet, in truth.
PubMed is our friend.The 20% fat advice does seem to work alright for me, for the most part, as i got what is considered improvements in lipoprotein particle sizes, a 31 point drop in small LDL, a 431 point increase in large HDL. This contradicts blanket statements on pro-paleo websites that eating less fat will increase small LDL and decrease large HDL.
I try to avoid blogs/non-peer-reviewed websites unless there is reason to believe a particular blogger/website writer has noted a problem in the peer-reviewed literature not noted by other peer-reviewed and published articles.The low white blood cell count is a normal finding on CR/very low BMI.
All in all, it looks like you're doing great!
Best,
GB
Re: Fidel's tests
(((Fidel))) I hear you on the care-taking. It makes it much harder to care for yourself- especially with regards to sleep when you are constantly vigilant. You are doing an amazing job with diet given all you are up against. Your diligence is commendable.
Nice summary of the two tests; thanks. It's good to know the first was from April. It helps to have a concise side-by-side comparison.
If your homocysteine continues to be high, you may want to check your methylation SNPs. If you've done 23andMe, you can really easily run your data at this site: https://geneticgenie.org/methylation-analysis/. If you carry a MTHFR mutation, you may need to supplement your Bs more diligently to bring that down. Dr. Ram from The Buck reports that amyloid plaque begins accumulating with levels above 6 umol/L
Forgive my continued questions, but I can't recall if you've revealed your gender and/or family history with re. to AD and CAD. It occurs to me, that especially with the new evidence from the AAIC conference that male and female E4 carriers may be on two separate journeys. Your specific approach may be very well-suited to your risks.
Nice summary of the two tests; thanks. It's good to know the first was from April. It helps to have a concise side-by-side comparison.
If your homocysteine continues to be high, you may want to check your methylation SNPs. If you've done 23andMe, you can really easily run your data at this site: https://geneticgenie.org/methylation-analysis/. If you carry a MTHFR mutation, you may need to supplement your Bs more diligently to bring that down. Dr. Ram from The Buck reports that amyloid plaque begins accumulating with levels above 6 umol/L
Forgive my continued questions, but I can't recall if you've revealed your gender and/or family history with re. to AD and CAD. It occurs to me, that especially with the new evidence from the AAIC conference that male and female E4 carriers may be on two separate journeys. Your specific approach may be very well-suited to your risks.
I couldn't agree more. I'm very much in favor of CRON for our allele, but for me it's all about walking a fine line. I feel best with my BMI around 18-18.5. Given the research that points to the efficacy of exercise as a neuroprotective strategy, I think it's vital to consume enough calories to be able to enjoy at least an hour of daily vigorous physical activity.People tell me I should be cautious letting my BMI get below 18.5. I tell them they should be cautious letting their BMI get above 18.5. (And we're both probably right! Caution is the watchword.)
July tests
Those are all good points, Gilgamesh.
Here are my calories numbers and saturated fat in grams, in reverse chronology for 31 days preceding the blood tests:
1764 6.8, 1693 6.3, 1803 7.0, 1818 7.0, 2006 7.1, 1844 12.8, 1605 6.0, 1800 5.9, 2124 7.9,
1744 7.2, 1530 4.6, 1873 4.1, 1905 12.5, 1402 4.8, 1423 6.0, 1846 5.3, 1804 5.3, 1793 5.2,
1992 4.6, 1811 13.2, 1723 7.3, 1696 7.6, 1856 7.2, 1793 7.8, 1681 6.1, 1806 9.1, 1731 13.1,
1601 10.9, 1641 6.6, 1496 6.4, 1720 7.7,
54324 calories in 31 days = 1752 average daily calories.
229.4 grams of saturated fat in 31 days = 7.4 average daily grams or 66.6 calories worth.
So my saturated fat was actually only 3.8% of my calories on average. That probably helped get my fasting glucose down. I just took another look at the mechanisms by which that happens at http://gg.gg/sat-fat_blood-sugar
I mentioned that a return to higher dietary fat might get my Lp(a) back to optimal. That is backed up by the study at http://gg.gg/low-fat_Lpa. Could have also said a return to lower dietary protein could help get that done due to a possible connection between homocysteine and Lp(a). After thinking that, came across this study about an interaction between the two increasing CAD risk: http://gg.gg/Hcy-Lpa
Apparently stress can be a factor in elevated homocysteine, so my being woken from sleep over and over could have played a role, since that is surely stressing.
Here are my calories numbers and saturated fat in grams, in reverse chronology for 31 days preceding the blood tests:
1764 6.8, 1693 6.3, 1803 7.0, 1818 7.0, 2006 7.1, 1844 12.8, 1605 6.0, 1800 5.9, 2124 7.9,
1744 7.2, 1530 4.6, 1873 4.1, 1905 12.5, 1402 4.8, 1423 6.0, 1846 5.3, 1804 5.3, 1793 5.2,
1992 4.6, 1811 13.2, 1723 7.3, 1696 7.6, 1856 7.2, 1793 7.8, 1681 6.1, 1806 9.1, 1731 13.1,
1601 10.9, 1641 6.6, 1496 6.4, 1720 7.7,
54324 calories in 31 days = 1752 average daily calories.
229.4 grams of saturated fat in 31 days = 7.4 average daily grams or 66.6 calories worth.
So my saturated fat was actually only 3.8% of my calories on average. That probably helped get my fasting glucose down. I just took another look at the mechanisms by which that happens at http://gg.gg/sat-fat_blood-sugar
I mentioned that a return to higher dietary fat might get my Lp(a) back to optimal. That is backed up by the study at http://gg.gg/low-fat_Lpa. Could have also said a return to lower dietary protein could help get that done due to a possible connection between homocysteine and Lp(a). After thinking that, came across this study about an interaction between the two increasing CAD risk: http://gg.gg/Hcy-Lpa
Apparently stress can be a factor in elevated homocysteine, so my being woken from sleep over and over could have played a role, since that is surely stressing.
3/4
