206 replies to this topic

[zoolander]

don't apologise.

The discussions have led me to review my supplement regime and that's always a good things

[zoolander]

I have added my blood biochemistry to my initial post. The blood biochemistry dates back to Nov 2006.

from most recent analysis,
NOTES: (from top to bottom)
1. Bilirubin levels are borderline high. This may be due to the volume of training I have been involved in. The blood was taken at week 4 of a GVT cycle. I have also increased the distance cycled per week to 80kms. I'll be watching this because high bilirubin levels may suggest liver issues. It may also be the result of some of the medications I am taking (see below)
2. I'm happy with my trigylceride levels. I changed from HDL/LDL cholesterol ratios and chose to go with Apolipoprotein measurements. I happy with the Apo B/ Apo A-1 ratio
3. FBE is normal
4. For some reason I didn't get the results for total and free T3 and T4. I am interested in these because I use thyroxine for the extra boost. The thyroxine use explains previous high values for free T4. I don't have a thyroid condition
5. Iron levels are high because of the Thyroxine. Thyroxine increases the metabolic rate and with this comes elevated Iron levels. This not exactly optimal considering that high iron = more free radicals. I'm taking a break from the thyroxine as a result.
6. B12 levels are high most likely because I supplement with 1000ug of Methylcolbalamin each morning Monday-Friday. I'm changing this to 3 x per week (Mon, Wed, Fri).

Special note should be taken to my blood biochemistry as a sign of what can happen when you introduce medications into your regime. Keeping tabs on blood biochemistry helps you keep values in control. It also gives you a objective look at your current health status.

Feedback and comments welcome

Edited by zoolander, 24 May 2008 - 05:43 AM.

[shuffleup]

2. You should try to get 30 minutes or so unprotected exposure without burning to the sun daily. Your vitamin D3 supplement simply won't boost D3 levels as effectively (or perhaps as safely--recent studies have linked exogenous Vitamin D supplementation with formation of calcium deposits on the brain and other internal organs). Mortality and incidence rates for most internal cancers, osteporosis etc. skyrocket with decreased sun exposure; this is now inarguable.

2400 IU would be too much for me. Vitamin D supplementation needs to be calibrated with blood testing.

Why would D supplementation be any more dangerous than getting sun, assuming that blood levels are kept in the optimal range?

A recent high profile study found a "strong association" between consumption of supplemental Vitamin D and calcium and the formation of dangerous brain lesions, even after accounting for all other mitigating factors.

Here's one article I quickly found discussing the study; I originally read about it elsewhere:

http://www.medicinen...rticlekey=80821

That's not to say there aren't benefits from exogenous supplementation of vitamin D that outweigh these risks, but they should be recognized, and consideration should be given to obtaining vitamin D to the extent possible through unprotected sun exposure (without burning).

The issue of whether Vitamin D supplementation without sun exposure is sufficient to ensure optimal vitamin D levels in the body is important to me personally, as my mother, who is 58 and a history professor at Loyola University in Baltimore MD, was diagnosed this year with a very advanced form of osteoporosis, a diagnosis she sought only after her shoulder broke this January while performing a simple movement in her ballroom dancing class. Vitamin D levels in her blood were found to be dangerously low, and her doctor prescribed several thousand IU of vitamin D daily as a supplement. However, my 105 lb mother had been taking 2,000 IU of vitamin D as a supplement for over 20 years, and enjoys dairy products as part of her normal diet on top of that.

What she hadn't been doing was getting ANY unprotected sun exposure during that period of time; although she had enjoyed sunbathing in her twenties, she kept up on current research at that time and concluded any unprotected sun exposure would accelerate aging of her skin and increase risk of skin cancer, without any benefits that couldn't be duplicated by taking supplemental vitamin D. I pleaded with her to reconsider starting in about 2004 as I started reading more and more studies conducted in low light countries and elsewhere (more recently, in the US too) finding a very high correlation between lack of sun exposure and greatly increased rates of incidence and mortality for most forms of internal cancers, as well as greatly increased rates for other diseases such as osteoporosis. My mother dismissed these concerns as "ridiculous." I wish she had listened to me then--she is now.

I tested my Vit D levels after taking about 4-5K IU's / day for a couple months. This was NOW's Olive oil based gelcap. I tested out at 42ng/dl if I recall correctly. This is in the OK range but on the lower end of the ref range. I hadn't gotten any significant sun exposure because this reading was taken in Jan. I now am taking about the same amount or up to 6K IU's except on days where I get some sun exposure.

I also supplement with Vit K2 MK-7 form. Would this address any of the calcificaiton issues you disucss?

[krillin]

I tested my Vit D levels after taking about 4-5K IU's / day for a couple months. This was NOW's Olive oil based gelcap. I tested out at 42ng/dl if I recall correctly. This is in the OK range but on the lower end of the ref range. I hadn't gotten any significant sun exposure because this reading was taken in Jan. I now am taking about the same amount or up to 6K IU's except on days where I get some sun exposure.

I also supplement with Vit K2 MK-7 form. Would this address any of the calcificaiton issues you disucss?

40-50 ng/ml seems optimal to me. The upper bound of the reference range of 32-100 ng/ml is irresponsible. I've yet to see any report of additional benefit to getting D above 50, and having 89 or above triples your risk of heart disease. K2 is good insurance against calcification.

Eur J Epidemiol. 2001;17(6):567-71.
Comment in: Eur J Epidemiol. 2003;18(5):461-2.
Serum 25-hydroxyvitamin D3 levels are elevated in South Indian patients with ischemic heart disease.
Rajasree S, Rajpal K, Kartha CC, Sarma PS, Kutty VR, Iyer CS, Girija G.
Department of Cardiology and Achutha Menon Centre for Health Science Studies, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India.

Several lines of evidence point to a possible relationship between vitamin D and cardiovascular disease. Animal experiments and observational studies in humans suggest vitamin D to be arteriotoxic and an association of high intake of vitamin D with increased incidence of ischemic heart disease (IHD). The major source of vitamin D in adults is vitamin D synthesized in the skin through exposure to the sun. In tropical environment there is a possibility of high level of solar exposure and enhanced serum levels of vitamin D in the population. We explored the relation between serum level of 25-hydroxyvitamin D3 and IHD in a case-control study involving 143 patients with either angiographic evidence of coronary artery disease or patients with acute myocardial infarction and 70 controls, all men in the age group of 45-65 years. Fasting blood samples were collected, serum separated and serum levels of 25-hydroxyvitamin D3 was measured by protein binding radioligand assay. Serum levels of cholesterol, triglyceride, calcium, magnesium and inorganic phosphate were also determined. Prevalences of diabetes, hypertension and smoking history were noted. Statistical comparisons of variables between cases and controls were done using chi2-tests. Multivariate logistic regression analysis was done to examine the association of IHD with serum levels of 25-hydroxyvitamin D3 controlling for selected variables. Serum levels of 25-hydroxyvitamin D3, calcium, inorganic phosphate, total cholesterol, low density lipoprotein and triglycerides were elevated in a higher proportion of patients, compared to controls. Serum levels of 25-OH-D3 above 222.5 nmol/l (89 ng/ml) was observed in 59.4% of cases compared to 22.1% in controls (p < 0.001; unadjusted odds ratio (OR): 5.17; 95% confidence interval (CI): 2.62-10.21). When controlled for age and selected variables using the multivariate logistic regression, the adjusted OR relating elevated serum 25-hydroxyvitamin D3 levels (> or = 222.5 nmol/l, > or = 89 ng/ml) and IHD is 3.18 (95% CI: 1.31-7.73). Given the evidences for the arteriotoxicity of vitamin D, further investigations are warranted to probe whether the elevated serum levels of 25-hydroxyvitamin D3 observed in patients with IHD in a tropical environment has any pathogenic significance.

PMID: 11949730

Med Hypotheses. 2007;68(5):1026-34. Epub 2006 Dec 4.
Vitamin D toxicity redefined: vitamin K and the molecular mechanism.
Masterjohn C.
Weston A. Price Foundation, 4200 Wisconsin Ave., NW, Washington, DC 20016, United States. ChrisMasterjohn@gmail.com

The dose of vitamin D that some researchers recommend as optimally therapeutic exceeds that officially recognized as safe by a factor of two; it is therefore important to determine the precise mechanism by which excessive doses of vitamin D exert toxicity so that physicians and other health care practitioners may understand how to use optimally therapeutic doses of this vitamin without the risk of adverse effects. Although the toxicity of vitamin D has conventionally been attributed to its induction of hypercalcemia, animal studies show that the toxic endpoints observed in response to hypervitaminosis D such as anorexia, lethargy, growth retardation, bone resorption, soft tissue calcification, and death can be dissociated from the hypercalcemia that usually accompanies them, demanding that an alternative explanation for the mechanism of vitamin D toxicity be developed. The hypothesis presented in this paper proposes the novel understanding that vitamin D exerts toxicity by inducing a deficiency of vitamin K. According to this model, vitamin D increases the expression of proteins whose activation depends on vitamin K-mediated carboxylation; as the demand for carboxylation increases, the pool of vitamin K is depleted. Since vitamin K is essential to the nervous system and plays important roles in protecting against bone loss and calcification of the peripheral soft tissues, its deficiency results in the symptoms associated with hypervitaminosis D. This hypothesis is circumstantially supported by the observation that animals deficient in vitamin K or vitamin K-dependent proteins exhibit remarkable similarities to animals fed toxic doses of vitamin D, and the observation that vitamin D and the vitamin K-inhibitor Warfarin have similar toxicity profiles and exert toxicity synergistically when combined. The hypothesis further proposes that vitamin A protects against the toxicity of vitamin D by decreasing the expression of vitamin K-dependent proteins and thereby exerting a vitamin K-sparing effect. If animal experiments can confirm this hypothesis, the models by which the maximum safe dose is determined would need to be revised. Physicians and other health care practitioners would be able to treat patients with doses of vitamin D that possess greater therapeutic value than those currently being used while avoiding the risk of adverse effects by administering vitamin D together with vitamins A and K.

PMID: 17145139

[krillin]

I have added my blood biochemistry to my initial post. The blood biochemistry dates back to Nov 2006.

Homocysteine is high. LEF likes it to be below 7.2. I'd add gram quantities of TMG to the regimen.

Your B12 isn't that high. Mine was too high to be measured, so it was reported as >2000 pg/ml.

[zoolander]

I've already considered TMG. I will more than likely order some with my next pay packet

[FunkOdyssey]

Zoo, its time to buy a didgeridoo!

BMJ 2006;332:266-270 (4 February), doi:10.1136/bmj.38705.470590.55 (published 23 December 2005)

Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial

Milo A Puhan, research fellow1, Alex Suarez, didgeridoo instructor2, Christian Lo Cascio, resident in internal medicine3, Alfred Zahn, sleep laboratory technician3, Markus Heitz, specialist in respiratory and sleep medicine4, Otto Braendli, specialist in respiratory and sleep medicine3

1 Horten Centre, University of Zurich, 8091 Zurich, Switzerland, 2 Asate Alex Suarez, 9630 Wattwil, Switzerland, 3 Zuercher Hoehenklinik Wald, CH-8639 Faltigberg-Wald, Switzerland, 4 Lungenpraxis Morgental, Zurich, Switzerland

Correspondence to: O Braendli otto.braendli{at}zhw.ch

Abstract

Objective To assess the effects of didgeridoo playing on daytime sleepiness and other outcomes related to sleep by reducing collapsibility of the upper airways in patients with moderate obstructive sleep apnoea syndrome and snoring.

Design Randomised controlled trial.

Setting Private practice of a didgeridoo instructor and a single centre for sleep medicine.

Participants 25 patients aged > 18 years with an apnoea-hypopnoea index between 15 and 30 and who complained about snoring.

Interventions Didgeridoo lessons and daily practice at home with standardised instruments for four months. Participants in the control group remained on the waiting list for lessons.

Main outcome measure Daytime sleepiness (Epworth scale from 0 (no daytime sleepiness) to 24), sleep quality (Pittsburgh quality of sleep index from 0 (excellent sleep quality) to 21), partner rating of sleep disturbance (visual analogue scale from 0 (not disturbed) to 10), apnoea-hypopnoea index, and health related quality of life (SF-36).

Results Participants in the didgeridoo group practised an average of 5.9 days a week (SD 0.86) for 25.3 minutes (SD 3.4). Compared with the control group in the didgeridoo group daytime sleepiness (difference -3.0, 95% confidence interval -5.7 to -0.3, P = 0.03) and apnoea-hypopnoea index (difference -6.2, -12.3 to -0.1, P = 0.05) improved significantly and partners reported less sleep disturbance (difference -2.8, -4.7 to -0.9, P < 0.01). There was no effect on the quality of sleep (difference -0.7, -2.1 to 0.6, P = 0.27). The combined analysis of sleep related outcomes showed a moderate to large effect of didgeridoo playing (difference between summary z scores -0.78 SD units, -1.27 to -0.28, P < 0.01). Changes in health related quality of life did not differ between groups.

Conclusion Regular didgeridoo playing is an effective treatment alternative well accepted by patients with moderate obstructive sleep apnoea syndrome.

[zoolander]

cheers funk.

There are a few modalities out there said to help with obstructive sleep apnea. Unfortunately for me these are sucessful with the mild to moderate types. I have the severe :(

[zoolander]

added Polypodium leucotomos extract for sun protection

Drugs Today (Barc). 2007 Jul;43(7):475-85.Click here to read Links
Polypodium leucotomos extract: a nutraceutical with photoprotective properties.
Gonzalez S, Alonso-Lebrero JL, Del Rio R, Jaen P.

Dermatology Service, Memorial Sloan-Kettering Cancer Center, New York, NY 10022, USA. gonzals6@mskcc.org

Ultraviolet (UV) irradiation causes multifaceted damage to the skin and adjacent tissue layers, and is one of the leading causes of premature skin aging, immunosuppression and carcinogenesis. Photoprotection can be achieved by the use of sunscreens and also by systemically administered compounds that fight the deleterious biological effects of UV exposure, or preferably both. In this review, we summarize the current knowledge on the tissue, cellular and molecular mechanisms underlying the photoprotective effect of Polypodium leucotomos fern extract. P. leucotomos blocked the deleterious effect of UV irradiation both in vivo and in vitro. The molecular basis of photoprotection relies on its ability to inhibit free radical generation, prevent photodecomposition of both endogenous photoprotective molecules and DNA, and prevent UV-induced cell death. Its complete loss of toxicity combined with its multifactor protection makes it a valuable tool not only for direct photoprotection, but also as an efficacious adjuvant to phototherapy of various skin diseases.

Added TMG (2g per day) to lower homocysteine levels (see blood biochemistry)

J Nutr. 2006 Jan;136(1):34-8.Click here to read Links

Orally administered betaine has an acute and dose-dependent effect on serum betaine and plasma homocysteine concentrations in healthy humans.
Schwab U, Törrönen A, Meririnne E, Saarinen M, Alfthan G, Aro A, Uusitupa M.

Department of Clinical Nutrition, University of Kuopio, Finland. Ursula.Schwab@uku.fi

Betaine, i.e., trimethylglycine, is linked to homocysteine metabolism. A 3-mo daily betaine supplementation decreased even normal plasma total homocysteine (tHcy) concentrations in humans. The pharmacokinetic characteristics and metabolism of betaine in humans have not been investigated in detail. The aim of this study was to assess the pharmacokinetics of orally administered betaine and its acute effect on plasma tHcy concentrations. Healthy volunteers (n = 10; 3 men, 7 women) with normal body weight (mean +/- SD, 69.5 +/- 17.0 kg), 40.8 +/- 12.4 y old, participated in the study. The betaine doses were 1, 3, and 6 g. The doses were mixed with 150 mL of orange juice and ingested after a 12-h overnight fast by each volunteer according to a randomized double-blind crossover design. Blood samples were drawn for 24 h and a 24-h urine collection was performed. Orally administered betaine had an immediate and dose-dependent effect on serum betaine concentration. Single doses of 3 and 6 g lowered plasma tHcy concentrations (P = 0.019 and P < 0.001, respectively), unlike the 1-g dose. After the highest dose, the concentrations remained low during the 24 h of monitoring. The change in plasma tHcy concentration was linearly associated with betaine dose (P = 0.006) and serum betaine concentration (R2 = 0.17, P = 0.025). The absorption and elimination of betaine were dose dependent. The urinary excretion of betaine seemed to increase with an increasing betaine dose, although a very small proportion of ingested betaine was excreted via urine. In conclusion, a single dose of orally administered betaine had an acute and dose-dependent effect on serum betaine concentration and resulted in lowered plasma tHcy concentrations within 2 h in healthy subjects.

Added L-Theanine to before bed stack. I'm suffering from sleep initiation insomnia before of my sleep apnea. I can't fall asleep with the mask on. Sticking to the therapy is important so I'm looking for supplements to help me get over this hurdle. I'm also using Phenibut and GABA every now and then to help.

Added skinceutical CE + Ferulic in morning skin care plus modified skin care regime (ala Fredrik)

Edited by zoolander, 03 June 2008 - 11:26 PM.

[Ben]

hi there, I wondering where you went to get such an extensive blood test. Did you just go to a GP and request a pathology script? If so what did you say? Cheers

Edit: Big thanks for posting your whole regimen, it must've taken you quite some time.

Edited by Ben - Aus, 04 June 2008 - 03:55 PM.

[zoolander]

added 100mg Aspirin. My reasoning for this is due to the increased risk of cerebro and cardiovascular problems that comes with having sleep apnea.

I also changed my cleanser from the 20% buffered glycolic acid to normal cetaphil. I've been experiencing a great deal of flaking for the last 3 weeks. Fredrik suggested that this may be due to increased cell turn over.

[zoolander]

removed the aspirin for the time being. I started bleeding in the eye. I've had this happen before with aspirin so I'm think that my blood is thin enough already. I may play around with the dosage at a later stage.

Edited by zoolander, 13 July 2008 - 12:21 AM.

[kismet]

Very interesting regimen and thank you for the references!
I just skimmed the whole discussion, but I didn't see anyone address the following:
(Assuming your regimen on the first page is up to date)
Chromium, the meta analysis you use as your reference showed no benefit or conflicting results as far as I can see.  It seems to work only in diabetics.

TMG/Betaine, do you think 2g, split up in 1g doses, is enough?
“The betaine doses of 3 and 6 g, but not 1 g, lowered homocysteine concentrations compared with the baseline concentrations”
Only the 6g dose was effective for the following 24h, 3g for ~7h. Even the higher dose resulted in only a modest decrease, I don't think 2g is enough. Are there any safety concerns with higher doses?

You use only 240mg Polypododium L. but Fredrik suggests 7.5mg/kg according to a study – about twice as much as you use. Is it because PL is expensive?
http://www.imminst.o...e-p-t22875.html

[happy]

Zoo,

I'm going to buy some protein powder.. am I better off buying Jarrow's from iherb or making a custom blend from true?

[zoolander]

making a custom powder will be better. You can add creatine, glutamine, taurine, leucine and so on

[zoolander]

I finally took the plunge

Now taking:

Ortho-core (AOR) 6 caps
R+ (SR) lipoic aicd (AOR) 150mg 2 caps

I also moved the EGCG extract into my with food supps as this is a lot easier on the liver

[krillin]

I finally took the plunge

Now taking:

Ortho-core (AOR) 6 caps
R+ (SR) lipoic aicd (AOR) 150mg 2 caps

I also moved the EGCG extract into my with food supps as this is a lot easier on the liver

All the cool people are taking quick release NaRALA now that we've realized it's a hormetic supplement. I mix the powder into water and then drink it on an empty stomach to maximize absorption. It starts out as sticky clumps but fully dissolves with some effort. I can imagine that encapsulated powder hitting stomach acid would polymerize like RALA, but I don't think anyone has done a comparison.

[brontesaurus]

Zoo,

In regards to your Casein-containg protein shake I found these posts from Duke back in 2005 talking negatively about casein, and I am wondering if there is any updated studies regarding the issues Duke brought up:

As for whey, while it is a fast digesting protein, that doesn't matter during daytime use, as long as you're getting protein every three hours (as your body doesn't store protein or amino acids like it does fat and glucose -- it needs to be replenished every three hours, which is why body builders eat so often). Casein is a slow digesting protein and often used by body builders for nighttime supplementation to prevent catabolic wasting, BUT casein is a cancer-promoting pro-aging supplement, and therefore I do not use it. Instead, I'll eat lean, free-range turkey breast at night for the same anti-catabolic effect.

I found this online excerpt from The China Study, relating to casein:
http://www.powerattu...article126.html

Here's a more hardcore article:
http://www.nature.co...l/7590997a.html

Yeah, practically nobody seems to be aware of the casein time bomb, even though there's been a lot of research worldwide showing its cancer promoting quality. This is why I avoid all dairy, with the exception of whey supplementation.

So many CRer's I know eat dairy, perhaps sabotaging their efforts. This, along with flax oil supplementation (laughably poor source of beneficial omega-3's, and known to encourage issues with the prostate and breast), are the two tragic mistakes I see CRer's make.

>>> those rats were fed AFLATOXIN.

Yes, and the researchers demonstrated that of these rats, the ones fed casein almost always developed cancer and died, while the rats fed other forms of protein did not. Casein itself DOES NOT cause cancer -- it ignites it into full-blown growth if you already have cancerous cells floating around in your body. So, it IS possible to consume casein and be okay, assuming you are generally cancer free to begin with.

As you get older, it's a foolish bet to take, though, since we ALL have some level of cancerous cells floating around in our body due to natural mutations. I'm not willing to take the risk that casein consumption might push some of those cells to take root and do real damage (which, btw, can be a very long-term effect, even decades, before the damage is noticeable).

Eat casein at your own risk -- it's like playing with fire.

... it's very hard to find protein bars that do not use casein because it's a cheap-as-dirt protein. Plus, I can't imagine any good protein bar being sold at Costco's. I shop there and Sam's and often look at the bars they sell, and they are ALL full of junk ingredients that you really want to avoid.

My view on casein is that while you may get away with eating it (just as some smokers live into their 90's), I prefer to eliminate all possible risk factors. This is why I consider myself much more hardcore about health than most people, as I'm perfectly willing to do whatever it takes, regardless of the price or the effort.

[zoolander]

Scott Miller (aka DukeNukem) is a perfectionist when it comes to his health and I commend him for this. I am familiar with Scott Millers take on Casein protein. I also understand why he feels that way. I'm guessing that his opinion is based on what he has read in the book "The China Study" as opposed to a review of the literature. Correct me if I am wrong .

If one were to review the literature they would find that the relationship between casein in the diet and cancer is not all that conclusive. Studies that have found and increase in tumorogenesis when a 20% casein diet was fed to animals are compounded by comparing the casein with other proteins that contain anticarcinogenic compounds. Soy for example contains phytosterols and isoflavonoids which inhibit tumor growth. A conclusion drawn from studies comparing a 20% casein diet with 20% soy diet where the incidence of cancer is 20% higher in the casein group could mean that the isoflavones and phytosterols in the soy diet decrease tumorogenesis suggesting that the casein is not tumorogenic instead, demonstrating that the soy is protective (1) On top of this there are studies where mice that were fed a 20% casein diet has a lower incidence of tumors when compared to mice fed the equivalent amount in mixed protein in their chow (2) as well as studies that show an increase (3).

As far as whey being a better protein than casein, well in what way? If Duke is suggesting that whey is not cancer promoting when compared to casein then he is not 100% correct in saying that. Bosselaers group concluded that casein, its pepsin hydrolysis products and BSA may protect mammalian cells against certain genotoxic compounds, whereas other milk proteins, such as whey protein, beta-lactoglobulin and soy protein, do not have this protective action (4).

So, it's not as black and white as saying that casein is bad and that whey is good. I chose the micellar casein based on the study that came out of Gaudichons lab that showed that the micellar casein has a slower rate of delivery of amino acids in the postprandial state when compared to the faster digesting proteins (5). This is why I also choose to take whey protein during the day and the micellar before bed.

I'd be interested in hearing from Scott on this one.

[Bghead8che]

Hi Zoolander,

Are you considering dropping Vinpocetine after the latest reports? I tried to look for a link to the recent post discussing Vinpocetine but could not find it. I was considering starting Vinpocetine but changed my mind.

-Brian

[zoolander]

I haven't had a chance to have a good read as yet. I'm about to place my 6-monthly order and hence will more than likely be reassessing my regime

[zoolander]

Added Ortho-Mind (6 caps per day) and removed some compounds due to double up
Added Jarrow Sleep optimizer (2 caps per day)

[thefirstimmortal]

pm

Edited by thefirstimmortal, 14 August 2008 - 05:59 AM.

[woly]

These two studies

Diets Containing Whey Proteins or Soy Protein Isolate Protect against 7,12-Dimethylbenz(a)anthracene-induced Mammary Tumors in Female Rats1
A study was conducted to determine the protective effects of two common dietary proteins, soy protein isolate (soy) and bovine whey, against chemically induced mammary tumors in female Sprague Dawley rats. Rats were fed AIN-93G diets having casein, soy, or whey as the sole protein source. Rats within the same dietary groups were mated to obtain the F1 and F2 generations. At age 50 days, F1 (experiment A) or F2 (experiment B) female offspring (19 rats/group) were p.o. gavaged with 80 mg/kg 7,12-dimethylbenz(a)anthracene, and mammary glands were evaluated when 100% of the casein-fed group developed at least one palpatable tumor. Rats grew well on all three diets, but casein-fed rats gained slightly more body weight than soy- or whey-fed rats (P < 0.05). Vaginal opening occurred 1 day earlier in soy-fed rats than in casein- or whey-fed rats, but no other differences in reproductive and developmental parameters were observed between groups. When 50% of the casein-fed rats had at least one mammary tumor, lower tumor incidences (24–34%) were observed in the soy-fed (P < 0.009) and whey-fed groups (P < 0.001). When 100% of the casein-fed rats had at least one tumor, soy-fed rats had a lower tumor incidence (77%) in experiment B (P < 0.002), but not in experiment A (P < 0.12), and there were no differences in tumor multiplicity. Whey-fed rats had lower mammary tumor incidence (54–62%; P < 0.002) and multiplicity (P < 0.007) than casein-fed rats in both experiments. Our results indicate that diets rich in soy reduce the incidence of chemically induced mammary tumors by approximately 20%. Furthermore, whey appears to be at least twice as effective as soy in reducing both tumor incidence and multiplicity.

and

Dietary Whey Protein Protects against Azoxymethane-induced Colon Tumors in Male Rats1
Epidemiological studies have suggested a relationship between diet and colon cancer incidence. Results from animal studies suggest that whey protein, but not casein protein, may provide protective effects against experimentally induced breast cancer in animals. In the current study, we investigated the effects of casein and whey diets on chemically induced colon cancer in male rats. Pregnant female Sprague Dawley rats (days 3–4 of gestation) were maintained on modified AIN-93G diets formulated with a single protein source of either casein or whey. Life-time exposure to these diets was studied in the F1 generation (experiment A) or the F2 generation (experiment B). Male offspring were weaned to the same diets as the dams and were maintained on these diets throughout the study. At age 90 days, all rats received azoxymethane once a week for 2 weeks (s.c., 15 mg/kg). Forty weeks after the last azoxymethane injection, all rats were euthanized, the colon was examined visually for tumors, and each tumor was histologically evaluated. The weights and distribution of all of the tumors were recorded. In experiment A, rats fed the casein diet had a 56% incidence of colon tumors compared with 30% of the rats on whey-based diets (P < 0.05). In experiment B, rats fed the casein diet had 50% incidence of colon tumors compared with 29% in the whey group (P < 0.05). There were no significant effects of diet on tumor multiplicity or mass. These results suggest that consumption of whey protein-containing diets may reduce the risk of developing colon tumors.

seem to suggest that atleast whey is probably better than casein. thoughts?

[zoolander]

Thanks for those references woly. Both whey and soy are great proteins. They both have their benefits. For example, soy protein has been shown to act as an insulin sensitiser (1) meaning it's a suitable protein for those with T2D and insulin sensitivity issues. Whey is also a great protein source and I don't need to post references if I were to say that whey protein (with resistance training) has been conclusively shown to support muscle protein synthesis. I'm a young healthy individual that lifts weights so my whey protein comes in handy.

[Bghead8che]

Thanks for those references woly. Both whey and soy are great proteins. They both have their benefits. For example, soy protein has been shown to act as an insulin sensitiser (1) meaning it's a suitable protein for those with T2D and insulin sensitivity issues. Whey is also a great protein source and I don't need to post references if I were to say that whey protein (with resistance training) has been conclusively shown to support muscle protein synthesis. I'm a young healthy individual that lifts weights so my whey protein comes in handy.

Please let me know if you decide to continue to go with Vinpocetine. I value your input.

-Brian

[Yann]

I always enjoy reading your posts Zoolander, I've learned a lot from them. I was wondering about your supplement cycling, why do you choose this specific cycling schedule? And do you also cycle the whey protein? Shouldn't whey protein powder be considered more a food than a supplement because it's a macronutrient?

[zoolander]

I did a few measurements today.

I've lowered the CHO content of my diet to well below 100g/day. It probably sits at below 50g/day. I have dramatically increased the fat content and consume about 30-50g of MCT from EVCO and about 25ml from EVOO. My protein content is at just over 2g/kg/bw.

Anyhow I weight myself this morning at the office in the fasted state using a Tanita BC-545

Weight:73.1kg
Body Fat %: 7.4%
Body Water: 66.5
Muscle Mass: 64.3kg
Bone Mass: 3.4kg

I was surprise by the drop in body fat % considering the fat content. I guess my fat phobia is invalid especially when referring to short and medium chain saturated fats.

Edited by zoolander, 14 January 2009 - 01:31 AM.

[zoolander]

I just did my lipid profile and flucose on the Cholestech LDX (unit = mmol/L)

Total Cholesterol: 4.2
HDL: 1.21
Triglycerides: 0.68
LDL: 2.68
non-HDL = 2.99
TC/HDL = 3.5

fasting Glucose: 3.88

10 year cardiovascular risk = 1%

[wayside]

Weight:73.1kg
Body Fat %: 7.4%
Body Water: 66.5
Muscle Mass: 64.3kg
Bone Mass: 3.4kg

I don't believe these numbers.

Googling around turns up the info that the male skeleton on average is about 15% of your body weight, which in your case would be 11 kg. If you are really lean that percentage is probably even higher. For this scale to say your bone mass is only 4.6% is almost certainly wrong.

So that means the other numbers are way off (except weight - that one is easy to get right); whether on the fat side or the muscle side, who knows? Although you can probably tell just be looking at yourself - 7.4% bf is pretty ripped, you should have a really nice 6 pack if you are that low.