Category Archives: NUTRITION & DIET

7 benefits of vitamin K you need to know about

https://www.top10homeremedies.com/news-facts/know-vitamin-k-important.html

CFC - Vitamin K

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All blog entries: Categorized with links

https://biotheorist.files.wordpress.com/2018/07/for-seekers-other-heretics-blog-entries-menu.pdf

SEEKERS & OTHER HERETICS MENU - CATEGORIZED WITH LINKS

 

Radio interview with the medical director of the largest private stem cell clinic in California

Click to access Denise Messenger’s 1-31-2018 radio interview with physician David Steenblock

DR Steenblock in blueDR S by bookcase SRI

1m51s video taken in and around Dr. Steenblock’s San Clemente, CA. clinic (Drone shots too)

31m (2011) video in which Dr. Steenblock discusses his use of adult (nonembryonic) stem cells & other modalities to treat chronic diseases & medical conditions (in adults & children):

 

How much vitamin C should one take?

Vitamin CRecently I was asked (on Facebook) how much vitamin C I take, which begs the question: What is the optimal intake of vitamin C for most people?

This is from my Facebook reply:

In order to answer this, I need to jump in the Way Back machine:

Back when I was studying for my doctorate in nutritional medicine (mid 1980s) there was a spirited debate going on among researchers, doctors, nutritionists and others concerning how much vitamin C a human being needed and could handle. Because I came into the realm of human nutrition with a background in biological anthropology (BS, MA) – training I actually undertook purposely not only because I dearly love bio anthro but also because I consider the insights and tools it provides foundational to understanding evolutionary players in human health & disease (and by virtue of this helpful in setting the stage for medical or paramedical studies) – I looked at the quantities of vitamin C produced in mammals that have retained the capacity to do so (Humans and many other primates such as gorillas lost this ability long ago). What emerged is that most nonhuman primates synthesis 25 mg of vitamin C per kilogram of body weight. If one applies this figure to an average (70 kg) human, this comes out to 1750 mg total daily.

There are, of course, mitigating factors. We know 70-90% of the vitamin C people get from food and supplemental forms are absorbed. However, too much taken all at one time reduces absorption! (If you take 1 gram of vitamin C only 50% will be absorbed). However, people with certain chronic diseases appear to absorb and use more even at high intakes.

With all this said, conventional thinking indicates that any amount of vitamin C over 180 mg daily will exceed what the tissues throughout the body can handle (i.e., saturation is reached) and the excess will be processed by the kidneys and dumped in the urine.

After years of dealing with people with chronic diseases, I have come to believe they should be taking 1750 mg to as much as 4 grams of vitamin C in divided doses daily (as their bodies can handle so much more C and apparently need this to support innate disease fighting processes). For healthy young to middle-aged folks, 180 mgs in divided doses or in slow or time release form should be adequate to meet the body’s demands for vitamin C.

Now to your specific question: How much C do I take daily? 500 mg Metabolic C in divided doses (100 mg every 3 hours from morning until evening). I take more than the 180 mg I mentioned above because I am getting older (62) and believe additional C is a good preventative measure as chronic disease processes are often subtlety at work (in even the healthiest of us) with increasing age.

Some folks argue for mega dosing – to “bowel tolerance” – whether healthy or not – which I think is a bit reckless (Most do it to “prevent various diseases especially cancer”). Vitamin C works as an antioxidant at low doses but can promote the production of ROS (reactive oxygen species) molecules when serum levels are very high. These ROS molecules can damage cell membranes and cause other biophysiological problems. As I recall, Nobel prize winning chemist Dr. Linus Pauling ingested mega doses of C daily for years on end. He lived to be 93 but died of prostate cancer. Some have argued his disease was triggered by his mega dosing on C. Dr. Pauling contended his high dose C kept his cancer at bay for years. One thing is certain: Years before Pauling’s’ demise, controlled studies were carried out to see if high dose C impacted various forms of cancer in animals and humans. The bottom line: It was ineffective. Advocates of high dose use of C rejected these studies for various reasons, while most of the scientific community accepted them as valid. The debate goes on to this day in various quarters

A parting word of advice: Do not “super mega dose” to prevent or treat disease. Those individuals reading this who have cancer and are considering using vitamin C to fight it should peruse https://www.cancer.gov/about-cancer/treatment/cam/patient/vitamin-c-pdq 

And so it goes……as do I…….

Of PQQ, Nutcracker Man & Tiger Nuts (PQQ as radioprotective with heart & nervous system benefits)

 

Pyrroloquinoline quinone - Wikpedia

Pyrroloquinoline quinone – Wikpedia

I have worked with a coenzyme called pyrroloquinoline quinone (PQQ) for quite a while now and think it is worth a “look see” by physicians and others for its preventative and therapeutic potential. Let’s dive into this now:

First, let’s “do the time warp, now”: During 1994-5 I worked in an Ag lab and large greenhouse complex outside Lincoln, Nebraska (Which was devoted to the testing of various nature-derived growth accelerants on culinary & medicinal mushrooms). One of the principle consulting researchers who rubbed elbows with me was Andy Anderson, PhD, who discovered a radioresistant bacterium back in 1956 while irradiating food at the Oregon Agricultural Experimental Station in Corvallis (As I recall from our chitchat, he was irradiating canned foods to see if this would reliably preserve them against spoilage). The bacterium was subsequently dubbed Deinococcus radiodurans and is indisputably the most radioresistant organism discovered to-date.

Read the rest of this entry

SHORT VIDEO: Options & Alternatives (Free pointers & help) by Choctaw Doc

Thumbnail 1:26

https://www.youtube.com/watch?v=9tR6iAHCcrc&feature=youtu.be

Reversing arterial blockage: Experimental regimen that worked for man facing amputation of his lower legs

Dr Payne at the Zeiss MicroscopeLast year (2012) I was contacted by a gentleman who had severe blockage in his legs and had been told by his physician-surgeon that he would need to amputate his legs below the knee. Naturally this chap was horrified at the prospect of living his life out of a wheelchair and/or on crutches and was frantic to know if there is anything, however experimental, that might help him avoid the surgeon’s knife. Apparently he had done a Google search and come across some of my health-related hypotheses (I have since 1986, been paid by various docs & researchers to spin hypotheses and provide novel ideas they could then pursue – or not).

I could not, of course, prescribe anything whatsoever as I am not a physician and lack the qualifications to get into such matters. However, what I did do is hand off an experimental regimen I originally developed in the late 1980s and had updated recently, along with the stringent caveat that much of my own work and that which informed it involved animal models of arterial blockage and I was giving him this with the strict understanding he would share it with his primary care MD and do what he said or advised.

I heard nothing from this chap for about 8 months and then got a call. It seems he was able to get his MD to endorse my handwork which he had followed religiously.  Long story short, the circulation in his legs had improved to the point that amputation was no longer on the proverbial table. Needless to say he and his wife of some 50+ years were overjoyed by his progress.

So here is what I shared with this guy – again, with the caveat it is experimental and unproved and should not be undertaken without the express consent & supervision of a duly licensed & practicing MD or DO.    

Dr. Anthony G. Payne

TO READ THE REST OF MY ARTICLE GO TO https://biotheorist.files.wordpress.com/2018/07/reversing-pad-cad-experimental-regimen-write-up-august-2013.pdf

Is cooking the main culprit behind the arterial blockage seen in the Horus mummies study?

Assorted fruitDuring March of this year (2013) a paper appeared in the journal The Lancet titled “Atherosclerosis across 4000 years of human history: the Horus study of four ancient populations”. You may have seen something about this among the many news articles and blurbs posted across the Web on the heels of this paper’s publication. If not, check out Science Daily’s excellent lay level piece on it at http://www.sciencedaily.com/releases/2013/03/130311091537.htm

 You can read the paper in its entirety at   http://download.thelancet.com/flatcontentassets/pdfs/S014067361360598X.pdf I perused it right after it came out and would like to share my thoughts on a possible culprit behind the arterial blockage that bedeviled the ancient peoples represented in the Horus study and which has cast a long shadow over modern populations as well (The fabled “Iceman“ Ötzi showed evidence of atherosclerosis too albeit he had a genetic predisposition and evidence of a chronic infection, namely borreliosis or Lyme disease).

CLICK THIS LINK TO READ THE REST OF THIS ARTICLE

 

 

Reading Room: Ketogenic Diet, Reducing Calcium in Arteries, Prostate Massage

LINKS TO LIVESTRONG.COM ARTICLES

CAM (Complimentary & Alternative Medicine)

 “Low Carb Ketogenic Diet” (LiveStrong.com)

“How to Reduce Calcium in Arteries” (LiveStrong.com)

CARDIOVASCULAR

 “How to Reduce Calcium in Arteries” (LiveStrong.com)

 DIET

 “Low Carb Ketogenic Diet” (LiveStrong.com)

PREVENTION

 “Low Carb Ketogenic Diet” (LiveStrong.com)

“How to Reduce Calcium in Arteries” (LiveStrong.com)

“Prostate Massage Methods” (LiveStrong.com)

 SEXUAL ISSUES

“Prostate Massage Methods” (LiveStrong.com)

 

 

Through the CAM looking Glass

Looking glass worldshttps://biotheorist.files.wordpress.com/2018/07/natural-medicine-a-cautionary-look.pdf

To slow aging => Reduce HIF-1 alpha (?)

Key protein may explain the anti-aging and anti-cancer benefits of dietary restriction

“Animals that were designed to over-express HIF-1 did not get the benefit of lifespan extension even though their diets were restricted. Animals that under-expressed HIF-1 lived longer, even when they had a nutrient-rich diet. Furthermore, it was found that the lifespan extension resulting from dietary restriction required activity in signaling pathways in the endoplasmic reticulum, the part of the cell involved in processing and the proper folding of proteins. This finding supports the theory that aging stems from the effects of misfolded proteins and opens up a rich area of investigation to examine the mechanisms by which stress in the endoplasmic reticulum affects lifespan”

Carcinogenesis. 2009 Apr;30(4):636-44. Epub 2009 Jan 8. Links

Grape seed extract inhibits VEGF expression via reducing HIF-1alpha protein expression.

Lu J, Zhang K, Chen S, Wen W.

Department of Molecular Medicine, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010, USA.

Grape seed extract (GSE) is a widely consumed dietary supplement that has antitumor activity. Here, we have investigated the inhibitory effect of GSE on the expression of vascular endothelial growth factor (VEGF) and the mechanism underlying this action. We found that GSE inhibited VEGF messenger RNA (mRNA) and protein expression in U251 human glioma cells and MDA-MB-231 human breast cancer cells. GSE inhibited transcriptional activation of the VEGF gene through reducing protein but not mRNA expression of hypoxia-inducible factor (HIF) 1alpha. The inhibitory effect of GSE on HIF-1alpha expression was mainly through inhibiting HIF-1alpha protein synthesis rather than promoting protein degradation. Consistent with this result, GSE-suppressed phosphorylation of several important components involved in HIF-1alpha protein synthesis, such as Akt, S6 kinase and S6 protein. Furthermore, in the MDA-MB-231 tumor, we found that GSE treatment inhibited the expression of VEGF and HIF-1alpha and the phosphorylation of S6 kinase without altering the subcellular localization of HIF-1alpha, correlating with reduced vessel density and tumor size. Depletion of polyphenol with polyvinylpyrrolidone abolished the inhibitory activity of GSE, suggesting a water-soluble fraction of polyphenol in GSE is responsible for the inhibitory activity. Taken together, our results indicate that GSE inhibits VEGF expression by reducing HIF-1alpha protein synthesis through blocking Akt activation. This finding provides new insight into the mechanisms of anticancer activity of GSE and reveals a novel molecular mechanism underlying the antiangiogenic action of GSE.

PMID: 19131542 [PubMed – indexed for MEDLINE]

PMCID: PMC2664452 [Available on 2010/04/01]

 Biochem Biophys Res Commun. 2009 Apr 24;382(1):96-101. Epub 2009 Feb 28. Links

D-glucosamine down-regulates HIF-1alpha through inhibition of protein translation in DU145 prostate cancer cells.

Park JY, Park JW, Suh SI, Baek WK.

Chronic Disease Research Center, School of Medicine, Keimyung University, 194 Dongsan-Dong, Jung-Gu, Daegu 700-712, Republic of Korea.

D-glucosamine has been reported to inhibit proliferation of cancer cells in culture and in vivo. In this study we report a novel response to D-glucosamine involving the translation regulation of hypoxia inducible factor (HIF)-1alpha expression. D-glucosamine caused a decreased expression of HIF-1alpha under normoxic and hypoxic conditions without affecting HIF-1alpha mRNA expression in DU145 prostate cancer cells. D-glucosamine inhibited HIF-1alpha accumulation induced by proteasome inhibitor MG132 and prolyl hydroxylase inhibitor DMOG suggesting D-glucosamine reduces HIF-1alpha protein expression through proteasome-independent pathway. Metabolic labeling assays indicated that D-glucosamine inhibits translation of HIF-1alpha protein. In addition, D-glucosamine inhibited HIF-1alpha expression induced by serum stimulation in parallel with inhibition of p70S6K suggesting D-glucosamine inhibits growth factor-induced HIF-1alpha expression, at least in part, through p70S6K inhibition. Taken together, these results suggest that D-glucosamine inhibits HIF-1alpha expression through inhibiting protein translation and provide new insight into a potential mechanism of the anticancer properties of D-glucosamine.

PMID: 19254699

 

Preventing or Slowing Liver Damage in Drinkers

silhouette of alcoholic drunk man drinking whiskey bottle feeling depressed falling into addiction problemAlcohol-induced disease is fairly commonplace among individuals who abuse alcohol. Fibrosis and cirrhosis by-and-large head the list. In both cases, abnormal changes take place in liver tissue that compromise this vital organ’s ability to function optimally. For many people who drink, a doctor’s finding of liver pathology (disease) is sufficient to get them to either curtail their drinking or abstain altogether (Whether on a temporary or permanent basis).

For others, however, a diagnosis of cirrhosis or other alcohol-induced disease does not put “the fear of God in ’em” with sufficient force for them to overcome the craving to elbow bend. What follows is information concerning a “dose of prevention” that may just spare the heavy drinker some grief down the line (Albeit this is by no means an argument to continue excessive drinking!)

This said, I would urge consistent moderate drinkers to pay attention to what I am about to share as well, as they too have the potential to experience liver damage over time that may not be readily repaired (and which could set the stage for problems later on in life).

A Dose of Prevention

In at least two separate animal studies carried out during the past fifteen years, a natural compound called lecithin protected animals who consumed booze in great quantities. Indeed, the animals were protected from developing many of the pathologic abnormalities common when alcohol is abused. Here are the details of this very compelling body of research:

In a study involving rats, 28 male littermates were pair-fed liquid diets containing 36% of energy either as ethanol (alcohol) or as additional carbohydrates for 21 days. Half of these rodents were given polyenylphosphatidylcholine (A component of lecithin) at 3 grams per liter of their food substrate (Liquid meals). The other group was given safflower oil (3 grams/liter) and choline (A chemical part of lecithin) as a bitatrate salt. The polyenylphosphatidylcholine (PPC) did not influence diet intake or alcohol consumption, but the booze-induced liver enlargement and accumulation of specific fats (lipids – triglycerides and cholesterol esters) and proteins were about half those in rats not given PPC. In rats that consumed PPC, post-eating rise in serum lipids was lower than was true of their littermates who had no PPC. The researchers, who worked at the Alcohol Research and Treatment Center, Bronx Veteran Affairs Medical Center (New York City), concluded that “These beneficial effects of PPC at the initial stages of alcoholic liver injury may prevent or delay the progression to more advanced forms of alcoholic liver disease” (1).

In a separate 10 year-long study involving baboons, also carried out at the Bronx Veteran Affairs Center (Section of Liver Disease and Nutrition), the suggested benefits of lecithin ingestion were even more encouraging.

In the study, twelve baboons (eight females, four males) were fed a liquid diet rich in alcohol supplemented with polyunsaturated lecithin (50% of total energy) or isocaloric carbohydrate. This group was compared with another group of eighteen baboons who were fed an equivalent diet (with or without alcohol), but without of lecithin. (2) Both groups developed increases in specific lipids (associated with alcohol use), but there were significant differences in the degree of liver injury (fibrosis) seen. For one thing, septal fibrosis (with cirrhosis in two animals) and transformation of their fat cells (lipocytes) into transitional cells developed in seven of the nine baboons fed the regular diet with alcohol. Septal fibrosis did not develop in any of the animals fed lecithin! In fact, they did not progress beyond the stage of perivenular (area around veins) fibrosis and had significantly lesser activation of fat cells to transitional cells. (3) The clincher came when the scientists took three of the lecithin-consuming animals off same but maintained their customary diet and alcohol mix. They very rapidly progressed to cirrhosis, accompanied by an increased transformation of their fat cells to transitional cells!

The fact these researchers found that choline exerted no protective effect in animals ingesting large quantities of alcohol led them to conclude that the polyunsaturated phospholipids might be responsible for the protective effect. This is underscored by the rodent study cited above, in which choline did not protect the animals from alcohol-induced liver damage, whereas PPC (Lecithin component) did. (4)

Baboon livers are remarkably similar to human livers (This is one reason an attempt was made many years back to transplant baboon livers into humans whose livers had failed). Given this, it seems logical that lecithin should provide human drinkers at least some of the benefits seen in the baboons. Accordingly, for those who drink — especially heavily — lecithin may be an invaluable form of health insurance. It is also easy on the pocketbook, being sold “dirt cheap” in health food and grocery stores plus pharmacies across the land.

In addition to lecithin, there are other compounds that if taken by drinkers should help reduce the damage to their livers.

For example, in alcoholics the conversion of the amino acid methionine to S-adensylmethionine (SAM-e) is significantly reduced. In baboon models of alcoholism, the animals experienced alcoholic cirrhosis that was opposed by replenishing SAM-e. Other lines of research indicate that bolstering SAM-e levels in human alcoholics decreases mortality, and offsets oxidative stress resulting from alcohol and alcohol byproduct induction of a liver detoxification enzyme designated cytochrome P4502E1 (CYP2E1).

SAM-e can readily be replenished by taking an oral form that reaches the bloodstream intact.

As the liver is a prime site for manufacture of one of the bodies most powerful antioxidants, glutathione, it logically follows that heavy use of alcohol would impact synthesis of this compound. And indeed, at least one animal study indicates this to be the case.

Fortunately, glutathione can be orally supplemented. However, not just any form of glutathione will work, as most forms are broken down in the gut and thus never reach the bloodstream intact. There are patented forms that resist breakdown until the glutathione has reached tissues throughout the body.

Of course, when it comes to drinking to excess – be it binge drinking or habitual heavy imbibing — curtailing or quitting is ideal. Those caught up in this sort of drinking pattern should seek professional help. But for addicts, alcohol abusers, and just plain ole social drinkers, offsetting some of the injury boozing does to the body (liver especially) is a prudent measure. The judicious use of lecithin, SAM-e and the right form of glutathione should readily help in this regard.

If only a small fraction of those who imbibe heavily take lecithin, SAM-e and glutathione benefit in terms of staving off the many diseases linked to alcohol abuse, the savings in terms of payouts for medical care and lost time from work alone could prove very substantial! This is a blessing to both the individual drinker and society at large.

See also: End stage cirrhosis reversed with nontoxic treatment

Dr. Anthony G. Payne

References

1. Navder KP, Baraona E, Lieber CS. ‘Polyenylphosphatidylcholine attenuates alcohol-induced fatty liver and hyperlipidemia in rats’. J. Nutrition, Sep;127 (9): 1800-6.
2. Liber CS, DeCarli LM, Mak KM, Kim CI, Leo MA. ‘Attenuation of alcohol-induced hepatic fibrosis by polyunsaturated lecithin’. Hepatology 1990 Dec;12 (6):1390-8 3. IBID 4. IBID
3. Liber, CS, ‘New Concepts of the pathogenesis of alcoholic liver disease lead to novel treatments, Curr Gastroenterol Rep 2004 Feb;6(1):60-5
4. Kessova IG, Ho YS, Thung S, Cederbaum AI, ‘Alochol-induced liver injury in mice lacking Cu, Zn-superoxide dismutase,’ Hepatology. 2003 Nov;38(5):1136-45
Original article upon which this piece is derived © 2003 by Dr. Anthony G. Payne. All rights reserved.

This article © 2010 by Dr. Anthony G. Payne. All rights reserved.

The information contained in this article is provided for informational purposes only and should not be construed as medical advice or instruction. Readers are advised to consult a licensed health care professional concerning all matters related to their health and well being

 

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