100 replies to this topic

[Sillewater]

kismet, on 28-Jun 2009, 05:21 AM, said:

Sillewater, on 28-Jun 2009, 02:23 AM, said:

So in rats they won't experience deficiencies because they have phytase that can break down the phytic acid.

Humans do not experience deficiencies either as studies clearly demonstrate (and even if they did: we couldn't care less as we have access to supplements). It's pointless to base speculation on a faulty premise, but anyway...
It doesn't matter if rats have phytase or not, controlled trials trump mechanistic speculation and rats apparently do accumulate IP6 and it's derivatives but only if they consume a diet with enough IP6 (i.e. the phytase is apparently not inactivating the IP6 as your hypothesis would require; alternatively, IP6 is re-synthesised from the break-down products). I don't have time to find out right now why your speculation is wrong (and I'm not sure what it's meant to imply), even though I'm very interested in destroying this myth more thoroughly. I'll be back in some weeks. 

Quote

Since humans have much lower levels, this could be why fiber prevents colon cancer, however I have read conflicting evidence, and I'm leaning towards fiber doesn't help at all (probably because of my paleo bias).

Fiber = undigestible carbohydrate != IP6. Although, I suppose that fiber intake can be a marker of IP6 intake as they're found in similar foodstuffs.

Quote

Would teeth be a good indicator of mineral deficiencies?

Not necessarily as there are many variables involved (sugar, hygiene, pathogens, etc). I believe bones are a better indicator and there's evidence in favour of IP6 there.

Well with the teeth I guess there are many variables involved and its true I haven't seen any studies pointing to IP6 causing deficiencies, just speculation.  

However in the study pointed out at the blog Whole Health Source the diet without grains reversed tooth decay the best, however I havent seen any controlled trials showing IP6 causing mineral deficiencies, but it does decrease the absorption of magnesium and calcium.

Quote

Decreased Absorption of Calcium, Magnesium, Zinc and Phosphorus by Humans due to Increased Fiber and Phosphorus Consumption as Wheat Bread1

John G. Reinhold2, Bahram Faradji3, Parichehr Abadi and Framarz Ismail-Beigi4
Medical Research Unit, Institute of Nuclear Medicine, Nemazee Hospital, and the Departments of Biochemistry and Medicine, School of Medicine, Pahlavi University, Shiraz, Iran

During a 20 day period of high fiber consumption in the form of bread made partly from wheaten wholemeal, two men developed negative balances of calcium, magnesium, zinc and phosphorus due to increased fecal excretion of each element. The fecal losses correlated closely with fecal dry matter and phosphorus. Fecal dry matter, in turn, was directly proportional to fecal fiber excretion. Balances of nitrogen remained positive. Mineral elements were well-utilized by the same subjects during a 20 day period of white bread consumption.

[Sillewater]

New blood test results:

Fasting Glucose : 5.2mmol/L (93.69mg/dL)
HbA1c: 4.6%

Cholesterol: 8.3mmol/L (320.46mg/dL)
HDL: 2.7mmol/L (104.25mg/dL)
LDL: 4.28mmol/L (165.25mg/dL) note: calculated
Triglycerides: 0.6mmol/L (53.1mg/dL)

Vitamin D: 150nmol/L (60.1ng/ml)

I would like my HbA1c to be lower, but I am happy with everything else. Any suggestions?

I eat a high fat low carb paleo diet. I exercise 3 times a week and fast 3 times a week.

[Athanasios]

Good stats.

I would recommend hiking as much as possible in those parks in N. Vancouver and eating at MoMo's Sushi at least twice a week.  

LUCKY! I visit whenever I can and it is pretty high on my list for places to move after finishing school.

[kismet]

Sillewater, on Jul 10 2009, 06:57 PM, said:

I would like my HbA1c to be lower, but I am happy with everything else. Any suggestions?

Blood sugar is rather good, but lipids suck. You should retest using a lipoprotein assay, though. Friedewald LDL estimates are probably inaccurate at low trig levels, but a HDL:LDL ratio which is not in the vicinity of 1, is, by all means, rather bad. Knowing the shortcomings of the LDL calculation is very important for paleo folks.  

Maybe stricht paleo is not such a good idea. Or at least eating strictly high-fat as JLL did (your diet might be similar):
http://inhumanexperi...sterol-and.html
The shortcomings of the Friedewald formula are mentioned later on in Eades' post:
http://www.proteinpo...myth/#more-3099

Edited by kismet, 10 July 2009 - 11:34 PM.

[Sillewater]

kismet, on Jul 10 2009, 04:32 PM, said:

Blood sugar is rather good, but lipids suck. You should retest using a lipoprotein assay, though. Friedewald LDL estimates are probably inaccurate at low trig levels, but a HDL:LDL ratio which is not in the vicinity of 1, is, by all means, rather bad. Knowing the shortcomings of the LDL calculation is very important for paleo folks.  

Maybe stricht paleo is not such a good idea. Or at least eating strictly high-fat as JLL did (your diet might be similar):
http://inhumanexperi...sterol-and.html
The shortcomings of the Friedewald formula are mentioned later on in Eades' post:
http://www.proteinpo...myth/#more-3099

I know the inaccuracy of Friedwald's formula for triglycerides under 100 (I keep up to date on Eades blog), but to get a direct test costs money right now, but I'll try and get one from my doctor soon. I should've stated that my calculated LDL is using the Iranian formula. But still its pretty high.

The things I like to keep track of is my triglycerides and HDL. Cause centenarians have higher and more fluffy HDL.

I read JLL's blog and have read his experiments. Interesting stuff. I always though triglycerides/HDL was a better predictor of heart disease because this ratio correlates with how much carbohydrate one consumes.

I know the lipids suck especially the high LDL, but I'm a cholesterol skeptic and I don't think cholesterol levels mean much, but I subscribe to Barry Groves statement about how if your cholesterol is lower than 7.0 mmol/L its a bad thing.

Peter at Hyperlipid discussed this paper:

Quote

Low admission LDL-cholesterol is associated with increased 3-year all-cause mortality in patients with non ST segment elevation myocardial infarction.

Al-Mallah MH, Hatahet H, Cavalcante JL, Khanal S.
Division of Cardiology, Henry Ford Heart and Vascular Institute, Detroit, MI 48202, USA. malmall1@hfhs.org
BACKGROUND: The relationship between admission low-density lipoprotein (LDL) levels and long-term outcomes has not been established in patients with acute coronary syndrome. We tested the hypothesis that patients who develop non-ST segment elevation myocardial infarction (NSTEMI) despite low LDL have a worse cardiovascular outcome in the long term. METHODS: Patients admitted with NSTEMI between 1 January 1997 and 31 December 2000 and with fasting lipid profiles measured within 24 hours of admission were selected for analysis. Baseline characteristics and 3-year all-cause mortality were compared between the patients with LDL above and below the median. Multivariate analysis was used to determine the predictors of all-cause mortality, and adjusted survival was analyzed using the Cox proportional hazard model. RESULTS: Of the total of 517 patients, 264 had LDL <or= 105 mg/dL and 253 had LDL > 105 mg/dL. There was no difference in age, gender, severity of coronary artery disease, and left ventricular ejection fraction between the 2 groups. Thirty-six percent of patients with LDL <or= 105 mg/dL and 24% of patients with LDL > 105 mg/dL were on lipid-lowering therapy on admission. After 3 years, patients with admission LDL <or= 105 mg/dL had higher all-cause mortality rate compared to patients with LDL > 105 mg/dL (14.8% vs. 7.1%, p = 0.005). The higher all-cause mortality persisted (OR 1.8, 95% CI 1.0-3.5, p = 0.05) even after adjustment for confounding variables. CONCLUSIONS: In our cohort, lower LDL-cholesterol at admission was associated with decreased 3-year survival in patients with NSTEMI. Whether this was a result of current therapy or a marker for worse baseline characteristics needs to be studied further.

Does LDL predict anything? I don't think so.

[Sillewater]

cnorwood, on Jul 10 2009, 04:29 PM, said:

Good stats.

I would recommend hiking as much as possible in those parks in N. Vancouver and eating at MoMo's Sushi at least twice a week.  

LUCKY! I visit whenever I can and it is pretty high on my list for places to move after finishing school.

I don't hike much but I have eaten at MoMo's a couple of times. Great sushi.

Maybe I'll start hiking!

Edited by Sillewater, 11 July 2009 - 05:48 AM.

[kismet]

Sillewater, on Jul 11 2009, 12:50 AM, said:

Does LDL predict anything? I don't think so.

I believe it does. It is considered a validated marker of CVD by evidence based medicine, whatever that is worth to you. It is considered to be very important by the sceptical Dr. Davis (although, lipoproteins are much more important according to him) who is also an advocated of low-moderate carb and paleolithic diets and CRONies generally have very low trigs and LDL. If your LDL is calculated using the Iranian formula already, then I think it is disastrous.

It is interesting to note that there seems to be a pretty good dose-response relationship between the magnitude of lipid lowering and outcomes (I don't have time to look up meta-analysis of epidemiology per se; statins have pleiotropic effects so one could argue that their other effects are responsible for improved outcomes but they still do correlate with the magnitude of LDL lowering...)

The relationship between reduction in low-density lipoprotein cholesterol by statins and reduction in risk of cardiovascular outcomes: an updated meta-analysis.
Delahoy PJ, Magliano DJ, Webb K, Grobler M, Liew D.
Clin Ther. 2009 Feb;31(2):236-44. Review.

Edited by kismet, 11 July 2009 - 05:47 PM.

[Sillewater]

kismet, on Jul 11 2009, 10:45 AM, said:

I believe it does. It is considered a validated marker of CVD by evidence based medicine, whatever that is worth to you. It is considered to be very important by the sceptical Dr. Davis (although, lipoproteins are much more important according to him) who is also an advocated of low-moderate carb and paleolithic diets and CRONies generally have very low trigs and LDL. If your LDL is calculated using the Iranian formula already, then I think it is disastrous.

It is interesting to note that there seems to be a pretty good dose-response relationship between the magnitude of lipid lowering and outcomes (I don't have time to look up meta-analysis of epidemiology per se; statins have pleiotropic effects so one could argue that their other effects are responsible for improved outcomes but they still do correlate with the magnitude of LDL lowering...)

The relationship between reduction in low-density lipoprotein cholesterol by statins and reduction in risk of cardiovascular outcomes: an updated meta-analysis.
Delahoy PJ, Magliano DJ, Webb K, Grobler M, Liew D.
Clin Ther. 2009 Feb;31(2):236-44. Review.

I started reading the THINCS website (their cholesterol skeptics) and then found Peter at Hyperlipid. the evidence he provides is pretty compelling and the discussions at THINCS are something everyone should read.

I understand that Dr. Davis thinks LDL should be below 60 (his 60-60-60 rule), but at Dr B.G. at Animal Pharm who probably helped Dr. Davis change the diet towards low-carb paleo diets focuses on the size of the particles and if triglycerides are low then LDL's will be big and fluffy (I will try and confirm this with a lipoprotein assay if my doctor will give me one).

Anyways on Dr. Davis' blog he mentioned the inaccuracy of the Friedwald equation. I do not know how accurate the Friedwald equation is the diets of American's today, because today we consume much more Omega 6, sugar, and carbohydrates, so I am thinking that would make the Equation more innacurate as discussed by Dr. Davis.

So the meta-analysis you provide could be based on erroneous LDL levels.

Here's a recent study showing that atheroma regression is not correlated with LDL (problems with this study is the small sample size and too short).

Quote

Safety and efficacy of achieving very low low-density lipoprotein cholesterol levels with rosuvastatin 40 mg daily (from the ASTEROID Study).

Wiviott SD, Mohanavelu S, Raichlen JS, Cain VA, Nissen SE, Libby P.
Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. swiviott@partners.org
Clinical trial evidence supports the use of intensive statin therapy for patients with coronary artery disease. High doses of potent statins have shown the greatest clinical benefit, but concerns persist regarding the efficacy and safety of achieving very low levels of low-density lipoprotein (LDL) cholesterol. We grouped patients treated with 40 mg of rosuvastatin daily by the LDL cholesterol achieved according to previous work (<40, 40 to <60, 60 to <80, 80 to <100, and > or =100 mg/dl) and by National Cholesterol Education Program targets (<70, 70 to <100, and > or =100 mg/dl) in A Study to Evaluate the Effect of Rosuvastatin on Intravascular Ultrasound-Derived Coronary Atheroma Burden (ASTEROID). The rates of key safety end points, including death, hemorrhagic stroke, and liver and muscle enzyme elevations, and key efficacy end points (atheroma burden) were compared using chi-square testing or Fisher's exact testing. The analysis included 471 patients who had had their LDL cholesterol measured at 3 months, of whom 340 (72.2%) had LDL cholesterol of <70 mg/dl, exhibiting excellent achievement of even the most stringent guideline-based goals. Of these 471 subjects, 192 (40.8%) had LDL cholesterol > or =40 mg/dl but <60 mg/dl, and 57 (12.1%) had LDL cholesterol <40 mg/dl. Adverse events occurred infrequently during the trial, and no pattern appeared relating the frequency of any adverse event to the achieved LDL cholesterol. Similarly, the on-treatment atheroma volume, change in atheroma volume, and high percentage of subjects with atheroma regression did not differ by the achieved LDL cholesterol. In conclusion, although the power to detect such changes was limited, these data showed no clear relation between the LDL cholesterol achieved by intensive statin therapy with rosuvastatin and adverse effects. Atheroma regression occurred in most patients and was not linked to the LDL cholesterol achieved.
PMID: 19576317 [PubMed - in process]

[kismet]

I just don't get why your cholesterol is so extremely high even though you are consuming a similar diet as JLL did. Do you have familial chol problems? Is there an obvious issue with your diet? I was always reluctant to review such biased and opiniated sources but if I get to it I'll take a look at their data, but the great majority of studies really seems to support a relation between LDL and heart disease. If we were wrong on such basic things like LDL, then I fear for evidence-based medicine... If only trig matters why not aim for 60-60-60 just to be sure?  

Edited by kismet, 11 July 2009 - 08:22 PM.

[Sillewater]

kismet, on Jul 11 2009, 01:21 PM, said:

I just don't get why your cholesterol is so extremely high even though you are consuming a similar diet as JLL did. Do you have familial chol problems? Is there an obvious issue with your diet? I was always reluctant to review such biased and opiniated sources but if I get to it I'll take a look at their data, but the great majority of studies really seems to support a relation between LDL and heart disease. If we were wrong on such basic things like LDL, then I fear for evidence-based medicine... If only trig matters why not aim for 60-60-60 just to be sure?  

Yea I don't know why my cholesterol is so high, I mean when compared to like Duke, JLL, Stephan at Whole Health Source, Richard at Free the Animal we all eat pretty similar diets, and their levels are all pretty similar.

But two others I know of that have my levels are Peter at Hyperlipid, and Barry Groves. My family does not have a history of familial cholesterol problems, so I am pretty sure its the diet.

I do eat a lot of butter, which Peter and Barry Groves also consume in high amounts. Peter also consumes like 6 egg yolks a day. I don't eat eggs everyday but when I do I consume around 6 egg yolks, but on average its probably 1 to 2 per day. Other than that my diet is a low-carb high-fat paleo diet.

I agree with you about the LDL I am still on the fence about it so I am a bit worried, so in a couple of months I will retest. But from the research I have read and from the THINCS community of cholesterol skeptics it does not look like LDL is causing heart disease.

In my laymans opinion inflammation and carbohydrate intake is more correlated to heart disease, and the reason it hasn't been fished out is that ppl lie about their carbohydrate intake.

I remember a study done on self-reported sugar intake, and it was determined through analysis of the urine that people always under-reported their sugar intake.

Edited by Sillewater, 11 July 2009 - 10:16 PM.

[nameless]

Have there been any heart disease studies where they measured people with mostly large particle LDL, but with various particle numbers, and if there was any heart disease correlation there?

It'd be interesting if Dr. Davis could comment on any of his patients with high-normal LDL, but everything else decent, and compare the results with the 60-60-60 people. Such as: 60-130-60 vs 60-60-60... would there be any difference in plaque reduction, assuming particle sizes, Lp(a) and inflammation are equal between the groups?

I'd also like to see more studies testing the correlation between HbA1c and heart disease. The only one I recall studied diabetics.

Edited by nameless, 11 July 2009 - 11:52 PM.

[Sillewater]

nameless, on Jul 11 2009, 04:52 PM, said:

Have there been any heart disease studies where they measured people with mostly large particle LDL, but with various particle numbers, and if there was any heart disease correlation there?

It'd be interesting if Dr. Davis could comment on any of his patients with high-normal LDL, but everything else decent, and compare the results with the 60-60-60 people. Such as: 60-130-60 vs 60-60-60... would there be any difference in plaque reduction, assuming particle sizes, Lp(a) and inflammation are equal between the groups?

I'd also like to see more studies testing the correlation between HbA1c and heart disease. The only one I recall studied diabetics.

I would also like to see more studies looking at HbA1c. Dr. Davis does focus a lot of his 60-60-60 mantra, but I have to say he does have a lot of experience. I might email him later.

Soon I will be getting Hcy and Lp(a) levels checked too.

And now I am no longer 21, I just turned 22.

[dbl]

You mentioned earlier in the thread that you eat 5-6 egg yolks per day. An egg yolk has over 200mg of cholesterol and the recommended limit is 300mg per day. That could explain your cholesterol issues.

[Sillewater]

dbl, on Jul 29 2009, 11:29 AM, said:

You mentioned earlier in the thread that you eat 5-6 egg yolks per day. An egg yolk has over 200mg of cholesterol and the recommended limit is 300mg per day. That could explain your cholesterol issues.

Well on average it probably turns out be be 2-4 egg yolks per day. But would dietary cholesterol cause serum cholesterol levels to rise like that?

Quote

Normal Plasma Cholesterol in an 88-Year-Old Man who Eats 25 Eggs a Day: Mechanisms of Adaptation (1991) Kern Jr, New England J Medicine 324(13):896-899

The effect of dietary cholesterol intake on serum cholesterol level is known to vary among individuals. The homeostatic and regulatory mechanisms which tend to keep serum cholesterol constant operate at different levels of efficiency in different individuals. An extreme case is reported here. A physician and colleagues from the University of Colorado School of Medicine have studied an 88-year-old man who, for ill-defined psychological reasons, has consumed 20 to 30 eggs daily for at least 15 years. This individual has maintained normal serum lipid levels and has no history of clinically important heart disease. He consented to participate in a variety of tests of cholesterol metabolism; the findings were compared with those obtained in an ongoing study of 11 normal volunteers who were tested while consuming normal diets and diets supplemented with five eggs per day. It was found that this individual had extremely efficient mechanisms that compensated for his phenomenally high cholesterol intake. In particular, he absorbed only 18 % of the cholesterol that he consumed; the comparison subjects absorbed 54.6% when on low-cholesterol diets and 46.4% when on high-cholesterol diets. He also showed a doubling of the usual rate of conversion of cholesterol to bile acids, moderately reduced cholesterol synthesis, and a possible increase in biliary cholesterol secretion. "These physiologic adaptations would leave little if any of the dietary cholesterol to elevate plasma cholesterol levels and be deposited in arterial walls."

According to this approximately 50% of the cholesterol is absorbed at higher intakes.

But maybe eating that much on a regular basis raises it pretty high.

[kismet]

Sillewater, on Jul 29 2009, 03:29 PM, said:

dbl, on Jul 29 2009, 11:29 AM, said:

You mentioned earlier in the thread that you eat 5-6 egg yolks per day. An egg yolk has over 200mg of cholesterol and the recommended limit is 300mg per day. That could explain your cholesterol issues.

Well on average it probably turns out be be 2-4 egg yolks per day. But would dietary cholesterol cause serum cholesterol levels to rise like that?

It never did anything to my cholesterol levels. At least not to this day. Cholesterol homeostasis seems to be pretty awesome while you are young. I suspect genetics play quite a role, though.

Edited by kismet, 29 July 2009 - 08:17 PM.

[kismet]

nameless, on Jul 11 2009, 07:52 PM, said:

It'd be interesting if Dr. Davis could comment on any of his patients with high-normal LDL, but everything else decent, and compare the results with the 60-60-60 people. Such as: 60-130-60 vs 60-60-60... would there be any difference in plaque reduction, assuming particle sizes, Lp(a) and inflammation are equal between the groups?

If Davis has <1000 patients I'd say the data would be worthless (ok, maybe n=100 would be enough, but his most recent open label trial involved ~30 patients IIRC).

Quote

I'd also like to see more studies testing the correlation between HbA1c and heart disease. The only one I recall studied diabetics.

Oh, boy, there's quite a story to be told about glucose and HbA1c (and it's pretty confusing). It's not just heart disease & diabetics. Again IIRC HbA1c - the lower the better, but fasting glucose shows a J-shaped response and ~90mg/dl seems like an optimal value. I suppose low HbA1c might better reflect low postprandial spikes and good insulin sensitivity.

[Sillewater]

Yea, from what I've seen the data is confusing. Especially the ones based on the Framingham Heart Study. They only find a relationship in women, not men.

While in other studies there is a relationship in men.

Good thing that the optimal is ~90mg/dL because low-carbers have that level.

[Sillewater]

Just wanted to update my Regimen as I have changed some things.

I'm beginning to take a more conservative stance on supplementation (thanks to Kismet for that). As a result I have backed off supplementing in a multi-vitamin type of way and decreasing my polyphenol intake, I have never subscribed to antioxidants being super beneficial, but I don't deny that they do have some health benefits.

I have also added a skin-care regimen, with related oral supplementation.

Fasting (I fast every third day for 24 hours)
Curcumin 665 mg
Lithium Orotate 4.9mg
ALCAR (588mg)
Resveratrol 300mg 98%
IP6 (1g)
Note: I take the Curcumin and Lithium Orotate the night before my fast. The Lithium dulls my mind so I take it before I sleep and when I take the curcumin on an emtpy stomach in the morning it doesn't feel like its absorbs well and I can feel it in my mouth.

Polyphenols
Now Foods, EGCg Green Tea Extract 400 mg
Pomegranate Extract
Grape Seed Extract
Note: I alternate these day by day, not taking them all at once on the same day.

Anti-glycation
Beta-alanine (its cheaper than Carnosine)
L-Taurine (this has other beneficial effects too)
Benfotiamine (80mg)
Pyridoxamine (50mg)/P5P
Note: I only take benfo and B6 on days I eat more than 80 grams of carbs. Usually occurs once a week.

Others
Piracetam
L-Theanine
Creatine Monohydrate (cheap stuff)

Multi-Vitamin
Fish Oil (EPA + DHA) w/ Vitamin E (mixed) (maybe Krill Oil instead)
Vitamin D3
Vitamin K2 3mg MK-4 and 45mcg MK-7 Note: I stopped with the 15mg of MK-4 because I find 3mg gives me the same effect on my teeth.
Vitamin C (1g time-released)
Magnesium Malate (500mg)
Note: I try to keep polyunsaturated fatty acids low so on days I take eat too much Omega 6, I take Omega 3 the next day and avoid Omega 6.

Adaptogens
Bacopa
Rhodiola
Ashwagandha
Maca
Note: I only buy one each time I run out of one of them. Currently using Maca, I like it.

Skin Care
Topical Vitamin E oil in the morning
Sunscreen (Filters: Mexoryl SX+XL, Stabilized Abovenzene, Tinsorb S+M)
Tretinoin (0.05% cream) at night every 3rd day

Oral
Xylitol
Carotenoids (Jarrows Carotenall)
Silicon (from oats and beer)

Whole Foods
Garlic
Ginger
Oats
Olive Oil
Blueberries

Diet Ratios:
1g of protein/kg of bodyweight
1.5-3.5g of fat/kg of bodyweight (half animal fat and half good vegetable fat, olive oil, avocado)
0.5-0.8g of carbohydrates/kg of bodyweight

Exercise:
Wind Sprints once a week
Bike to work
Resistance exercise twice per week

I exercise on Fast Days and I avoid all antioxidants on those days.

Edited by Sillewater, 18 August 2009 - 07:18 AM.

[Sillewater]

Updated Regimen:

Fasting Supplements (2x per week)
Lithium Orotate (5mg elemental lithium)
Resveratrol (200mg)
Curcumin (665 mg)

Multi-vitamin
Vitamin D3 (5000IU)
Vitamin K2 - MK7(90mcg)/MK4(5mg)
Magnesium Citrate (200mg)
Flax Seed Oil (3g)
CDP-Choline (250 mg)

Anti-glycation
P5P (100mg)
L-Lysine (500mg)
L-Arginine (500mg)

Whole Food Extracts
Pomegranate Extract (Punicalagins STD 120mg)

Fitness
Creatine Monohydrate (5g)
Beta-Alanine (2g)
Whey Protein Isolate (30g) on workout days: 2-3x per week

Other
Acetyl-L-Carnitine (500mg)
IP6 (500mg)
Xylitol Gum
Grape Seed Extract (100mg)

Probiotic
Jarrow Probiotic 1/week

Whole Foods
Green Tea Powder
Oats
Blueberries
Dark Chocolate (85% and above)
Garlic
Coconut Milk
Olive Oil
Nuts
Ginger Candies

[kismet]

Did you check whether the doses of lys/arg are high enough, particularly lys? Xylitol is only benefical at higher doses (6-10g), at lower doses it will have a minuscle or neutral effect. Why such low protein intakes? And don't forget not all nuts are created equal; walnuts, for instance, are extremely rich in PUFA.

Edited by kismet, 17 November 2009 - 03:42 PM.

[Sillewater]

kismet, on Nov 17 2009, 07:42 AM, said:

Did you check whether the doses of lys/arg are high enough, particularly lys? Xylitol is only benefical at higher doses (6-10g), at lower doses it will have a minuscle or neutral effect. Why such low protein intakes? And don't forget not all nuts are created equal; walnuts, for instance, are extremely rich in PUFA.

thanks Kismet, always very helpful.

I got the lys/arg for free. What I'm afraid of is the arginine affecting my NO synthesis down the line. I was going to look into whether lysine affects arginine in that way.

I chew the gum because it tastes good, and i also throw some xylitol (about 2g) into my oatmeal. Then I throw some into my desert at night (cream, coconut milk, one raw egg yolk, yoghurt, blueberries, xylitol, flax seed oil). So in a day I eat about 5g or a bit more.

My protein intake right now is around 1.5g/kg of body weight. I take the 30g post-workout, and for the rest of the day my protein intake is from meat. On days I don't workout (5 out of 7 days) I eat take in less protein, around 1.0-1.2g/kg (about 1/4 coming from plant sources).

For the nuts I don't eat walnuts, hate the taste. I just eat almonds, cashews, macadamia, and sometimes pistachios.

[Sillewater]

Simplified Regimen for 2010

Fasting Supplements
Curcumin (665mg)

Vitamins/Minerals
Vitamin A (5000IU)
Vitamin D3 (4000IU)
Vitamin K2 - MK7(90mcg)/MK4(5mg) [Alternate]
Magnesium Citrate (200mg)
Lithium Orotate (1mg/day)

Nootropic
CDP-Choline (250 mg)
Piracetam

Post-Prandial Protection (20 min before major meal)
P5P (100mg)
Na-R-Alpha Lipoic Acid (150 mg)
Carnosine (500mg)/Taurine (500mg) [Alternate]

Whole Food Extracts
Wine Concentrate (Wine Rx)
Flax Seed Oil (6g)

Other
IP6 (500mg)
Now Foods Gr8-Dophilus

Diet:
20:20:60 (C:P:F)
Fast 24 hrs every third day. I am sure that I am on some sort of calorie restriction as I have lost about 15 pounds over the last couple of months. It doesn't seem like its muscle mass but who knows. I have trouble reaching RDA's of folate, niacin and calcium which I will try and address by adding some legumes to my diet.

[kismet]

One thing I am wondering about--
Why do you take 250mg CDP-choline? It is usually taken w/ piracetam, but is it evidence based? Wouldn't regular choline do? (and your diet should be high enough in choline if you include eggs, although, CDP-choline does circumvent [the most] rate-limiting steps in PC synthesis)

I don't even know why  MR takes 500mgwhen many studies suggest benefits only at > or = 1000mg.

[meursault]

These are the studies I see most commonly cited for use of cdp-choline as a nootropic:

Quote

Citicoline: update on a promising and widely available agent for neuroprotection and neurorepair.

Saver JL.

UCLA Stroke Center and Department of Neurology, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.

Choline precursors promote repair and growth of cell membranes and hold promise in a variety of neurologic diseases, including ischemic and hemorrhagic stroke. Citicoline, the most well-studied choline agent precursor, is widely prescribed throughout the world and recently became available in the United States as a dietary supplement. In experimental stroke models, citicoline conferred acute neuroprotection and enhanced neuroplasticity and neurorepair in the subacute period. Although individual human stroke trials have been inconclusive, meta-analysis of 10 trials enrolling 2279 patients suggests patients receiving citicoline had substantially reduced frequencies of death and disability. Reinvestigation of citicoline with modern neuroimaging and clinical trial methods are underway and will provide more definitive information regarding the mechanistic and clinical effects of this promising neurotherapeutic agent.

Quote

Oral administration of circulating precursors for membrane phosphatides can promote the synthesis of new brain synapses.

Cansev M, Wurtman RJ, Sakamoto T, Ulus IH.

Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA, USA.

Although cognitive performance in humans and experimental animals can be improved by administering omega-3 fatty acid docosahexaenoic acid (DHA), the neurochemical mechanisms underlying this effect remain uncertain. In general, nutrients or drugs that modify brain function or behavior do so by affecting synaptic transmission, usually by changing the quantities of particular neurotransmitters present within synaptic clefts or by acting directly on neurotransmitter receptors or signal-transduction molecules. We find that DHA also affects synaptic transmission in mammalian brain. Brain cells of gerbils or rats receiving this fatty acid manifest increased levels of phosphatides and of specific presynaptic or postsynaptic proteins. They also exhibit increased numbers of dendritic spines on postsynaptic neurons. These actions are markedly enhanced in animals that have also received the other two circulating precursors for phosphatidylcholine, uridine (which gives rise to brain uridine diphosphate and cytidine triphosphate) and choline (which gives rise to phosphocholine). The actions of DHA aere reproduced by eicosapentaenoic acid, another omega-3 compound, but not by omega-6 fatty acid arachidonic acid. Administration of circulating phosphatide precursors can also increase neurotransmitter release (acetylcholine, dopamine) and affect animal behavior. Conceivably, this treatment might have use in patients with the synaptic loss that characterizes Alzheimer's disease or other neurodegenerative diseases or occurs after stroke or brain injury.

Quote

Citicoline enhances frontal lobe bioenergetics as measured by phosphorus magnetic resonance spectroscopy.

Silveri MM, Dikan J, Ross AJ, Jensen JE, Kamiya T, Kawada Y, Renshaw PF, Yurgelun-Todd DA.

Cognitive Neuroimaging Laboratory, McLean Hospital & Harvard Medical School, 115 Mill Street, Belmont, MA 02478-9106, USA. msilveri@mclean.harvard.edu

Citicoline supplementation has been used to ameliorate memory disturbances in older people and those with Alzheimer's disease. This study used MRS to characterize the effects of citicoline on high-energy phosphate metabolites and constituents of membrane synthesis in the frontal lobe. Phosphorus ((31)P) metabolite data were acquired using a three-dimensional chemical-shift imaging protocol at 4 T from 16 healthy men and women (mean +/- SD age 47.3 +/- 5.4 years) who orally self-administered 500 mg or 2000 mg Cognizin Citicoline (Kyowa Hakko Kogyo Co., Ltd, Ibaraki, Japan) for 6 weeks. Individual (31)P metabolites were quantified in the frontal lobe (anterior cingulate cortex) and a comparison region (parieto-occipital cortex). Significant increases in phosphocreatine (+7%), beta-nucleoside triphosphates (largely ATP in brain, +14%) and the ratio of phosphocreatine to inorganic phosphate (+32%), as well as significant changes in membrane phospholipids, were observed in the anterior cingulate cortex after 6 weeks of citicoline treatment. These treatment-related alterations in phosphorus metabolites were not only regionally specific, but tended to be of greater magnitude in subjects who received the lower dose. These data show that citicoline improves frontal lobe bioenergetics and alters phospholipid membrane turnover. Citicoline supplementation may therefore help to mitigate cognitive declines associated with aging by increasing energy reserves and utilization, as well as increasing the amount of essential phospholipid membrane components needed to synthesize and maintain cell membranes. Copyright © 2008 John Wiley & Sons, Ltd.

[Sillewater]

I have tried other forms of choline before and they didn't do anything, so I decided to give CDP-Choline a try and I can really feel a difference with this form (even at 250mg). I just wanted to try it and it seems it works so I might keep it in the regimen. Maybe it was because of my higher intake of eggs before that the other forms of choline didn't do anything (nowadays I only eat 3-4 egg yolks per week), but I see that many others on this forum and others respond to CDP-Choline very well.

[nito]

Sillewater, on Jan 5 2010, 04:05 PM, said:

I have tried other forms of choline before and they didn't do anything, so I decided to give CDP-Choline a try and I can really feel a difference with this form (even at 250mg). I just wanted to try it and it seems it works so I might keep it in the regimen. Maybe it was because of my higher intake of eggs before that the other forms of choline didn't do anything (nowadays I only eat 3-4 egg yolks per week), but I see that many others on this forum and others respond to CDP-Choline very well.

U feel at 250 mg? Is this on an empty stomach taken sublingually(under the tounge)? I don't feel it even if i take 1000mg of CDP.

[Sillewater]

Yea, I take it on an empty stomach.

[kismet]

Sillewater, on Jan 6 2010, 02:09 PM, said:

Yea, I take it on an empty stomach.

I am not sure you should feel CDP, but for actual benefits a dose from 500-2000mg seems prudent. The stroke studies from czukle's first abstract usually use 1k or 2k mg. Czukle's last references, however, is interesting and surprising ("These treatment-related alterations in phosphorus metabolites were not only regionally specific, but tended to be of greater magnitude in subjects who received the lower [500mg] dose."). Thought we have only animal studies on phospholipid metabolism.
Maybe that's a reason to up your intake?

Any idea who's offering the "best" taurine? Come to think of it, taurine seems pretty "paleo" to me. It's found in very high concentrations in some organs we'd normally not consume and the high-dose studies are pretty interesting too (but I don't think any population really consumes such high levels in the 1-3g/d range, so I'll personally stick to approx. 500mg/d).
Out of interest: are there good estimates of the meat consumption of paleolithic men or hunter-gatherers? Fish consumption? Any calculations as to their taurine intakes?

Edited by kismet, 06 January 2010 - 09:59 PM.

[FunkOdyssey]

They felt the cdp-choline when it caused anxiety (13.7% vs. 9.9% on placebo) and leg edema (9.7% vs. 6.5% placebo) in a clinical trial of stroke patients.  http://stroke.ahajou...eaha;33/12/2850

(to be fair it improved depression and reduced falls in the same population)

[Sillewater]

Maybe it was it being used with piracetam? I used to take piracetam without the choline and no other choline ever affected me. Or it could just be a placebo effect. I'll try 500mg, but would that include the choline I get from my diet? Because that is what I'm basing my 250mg dosage on. I get around 650-750mg from my diet. So 250 brings it up to those used in some of the studies I read. Or is CDP-Choline metabolized differently?

Here's some studies on meat consumption, I have no idea if they are good estimates though but if combined with isotopic studies that skotkonung knows about we should get a pretty good idea.

Quote

Eur J Clin Nutr. 2002 Mar;56 Suppl 1:S42-52.
The paradoxical nature of hunter-gatherer diets: meat-based, yet non-atherogenic.
Cordain L, Eaton SB, Miller JB, Mann N, Hill K.

Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, USA. cordain@cahs.colostate.edu
OBJECTIVE: Field studies of twentieth century hunter-gathers (HG) showed them to be generally free of the signs and symptoms of cardiovascular disease (CVD). Consequently, the characterization of HG diets may have important implications in designing therapeutic diets that reduce the risk for CVD in Westernized societies. Based upon limited ethnographic data (n=58 HG societies) and a single quantitative dietary study, it has been commonly inferred that gathered plant foods provided the dominant energy source in HG diets. METHOD AND RESULTS: In this review we have analyzed the 13 known quantitative dietary studies of HG and demonstrate that animal food actually provided the dominant (65%) energy source, while gathered plant foods comprised the remainder (35%). This data is consistent with a more recent, comprehensive review of the entire ethnographic data (n=229 HG societies) that showed the mean subsistence dependence upon gathered plant foods was 32%, whereas it was 68% for animal foods. Other evidence, including isotopic analyses of Paleolithic hominid collagen tissue, reductions in hominid gut size, low activity levels of certain enzymes, and optimal foraging data all point toward a long history of meat-based diets in our species. Because increasing meat consumption in Western diets is frequently associated with increased risk for CVD mortality, it is seemingly paradoxical that HG societies, who consume the majority of their energy from animal food, have been shown to be relatively free of the signs and symptoms of CVD. CONCLUSION: The high reliance upon animal-based foods would not have necessarily elicited unfavorable blood lipid profiles because of the hypolipidemic effects of high dietary protein (19-35% energy) and the relatively low level of dietary carbohydrate (22-40% energy). Although fat intake (28-58% energy) would have been similar to or higher than that found in Western diets, it is likely that important qualitative differences in fat intake, including relatively high levels of MUFA and PUFA and a lower omega-6/omega-3 fatty acid ratio, would have served to inhibit the development of CVD. Other dietary characteristics including high intakes of antioxidants, fiber, vitamins and phytochemicals along with a low salt intake may have operated synergistically with lifestyle characteristics (more exercise, less stress and no smoking) to further deter the development of CVD.

PMID: 11965522 [PubMed - indexed for MEDLINE]

And some speculation:
http://www.beyondveg...terview1g.shtml
http://www.marksdail...that-much-meat/

@Kismet,

That's interesting, I've never thought about purity issues with Taurine. I get mine from a sales rep I know that work's for ALLMAX (a sports supplement company in Canada) and it says Pharmaceutical Grade on it. But I'll definitely ask the rep next time I see him. (I currently work part-time at a natural health products store, I get a lot of free stuff, don't take most of it though.)

Edited by Sillewater, 07 January 2010 - 07:14 AM.