Would a Low Carb Diet Help with a Hair Regrowth Regimen?

[wookster]

http://www.thepaleodiet.com/published_r ... /#syndrome

http://www.thepaleodiet.com/articles/Hy ... 0Final.pdf

24. Cordain L, Eades MR, Eades MD. Hyperinsulinemic diseases of civilization: more than just syndrome X. Comp Biochem Physiol Part A 2003;136:95-112.

ABSTRACT

Compensatory hyperinsulinemia stemming from peripheral insulin resistance is a well recognized metabolic disturbance that is at the root cause of diseases and maladies of Syndrome X (hypertension, type 2 diabetes, dyslipidemia, coronary artery disease, obesity, abnormal glucose tolerance). Abnormalities of fibrinolysis and hyperuricaemia also appear to be members of the cluster of illnesses comprising Syndrome X. Insulin is a well established growth promoting hormone, and recent evidence indicates that hyperinsulinemia causes a shift in a number of endocrine pathways that may favor unregulated tissue growth leading to additional illnesses. Specifically, hyperinsulinemia elevates serum concentrations of free insulin like growth factor 1 (IGF-1) and androgens while simultaneously reducing insulin like growth factor binding protein 3 (IGFBP-3) and sex hormone binding globulin (SHBG). Since IGFBP-3 is a ligand for the nuclear retinoid X receptor ?, insulin mediated reductions in IGFBP-3 may also influence transcription of anti-proliferative genes normally activated by the body’s endogenous retinoids. These endocrine shifts alter cellular proliferation and growth in a variety of tissues whose clinical course may promote acne, early menarche, certain epithelial cell carcinomas, increased stature, myopia, cutaneous papillomas (skin tags), acanthosis nigricans, polycystic ovary syndrome (PCOS) and male vertex balding. Consequently, these illnesses and conditions may, in part, have hyperinsulinemia at their root cause and therefore should be classified among the diseases of Syndrome X.

 

[Nathaniel]

This study supports the notion that if you are insulin resistant (either from bad eating habits leading to diabetes 2 and obesity) this may make you more prone to balding.

However male pattern baldness is a side effect of hyperinsulinemia (which is caused by insulin resistance) and this is a totally different condition from having normal insulin release. So in a nutshell, you will only benefit from restricting carbs if you are hyperinsulinemic yourself.

 

[wookster]

:dunno:

Exactly how much insulin is too much and what is the optimal insulin levels for health, hair, and body-weight?

http://www.sciencedaily.com/releases/20 ... 120729.htm

ScienceDaily (Mar. 20, 2008) — Researchers at the Joslin Diabetes Center have shown that insulin has a previously unknown effect that plays a role in aging and lifespan, a finding that could ultimately provide a mechanism for gene manipulations that could help people live longer and healthier lives.

The paper, published in the March 21st issue of Cell, reports that insulin inhibits a master gene regulator protein known as SKN-1, and that increased SKN-1 activity increases lifespan. SKN-1 controls what is called the Phase 2 detoxification pathway, a network of genes that defends cells and tissue against oxidative stress -- damage caused by elevated levels of free radicals (byproducts of metabolism) -- and various environmental toxins. The new finding was demonstrated in experiments on the digestive system of C. elegans, a microscopic worm often used as a model organism.

"We've found something new that insulin does and it has to be considered when we think about how insulin is affecting our cells and bodies," said Dr. T. Keith Blackwell, senior investigator at Joslin and author of the paper. "This has implications for basic biology since under some circumstances insulin may reduce defense against the damaging effects of oxidative stress more than we realize."

[...]

"The major implication is that we have found something new that affects lifespan and aging, and an important new effect that insulin and/or a related hormone called insulin-like growth factor-1 may have in some tissues," said Blackwell. "The implications go far beyond diabetes."

It has been known since the 1990s that insulin inhibits a gene regulator protein known as FOXO, important in diabetes metabolism, tumor suppression and stem cell maintenance. FOXO controls a number of genes, including many involved in stress resistance. Studies in C. elegans showed that reduced insulin signaling boosted activity of a FOXO protein known as DAF-16, leading to greater stress resistance and longer life.

[...]

http://www.sciam.com/article.cfm?id=mit ... utations-b

Mitochondrial Mutations Blamed for Aging

[...]

Aleksandra Trifunovic of the Karolinska Institute in Sweden and her colleagues genetically engineered a line of mice to carry a compromised version of an enzyme called DNA polymerase-gamma, which normally proofreads mitochondrial DNA to ensure proper replication and aids in DNA repair. Subsequent tests of the transgenic animals¿ brain, heart and liver cells revealed three to five times as many errors in their mtDNA as in that of normal mice. By 25 weeks of age, young adulthood for rodents, the mutants began to develop hallmark signs of aging, including heart problems, osteoporosis, baldness and reduced fertility. None of them lived more than 60 weeks, the researchers report today in Nature. Normal mice, in contrast, live 100 weeks on average. Future experiments can use the prematurely aging mice to study how growing old "can be counteracted by genetic, pharmacological, or dietary interventions," the team writes.

http://www.ncbi.nlm.nih.gov/pubmed/18466343

The ketogenic diet increases mitochondrial glutathione levels.Jarrett SG,

Milder JB, Liang LP, Patel M.

Department of Pharmaceutical Sciences, University of Colorado Denver, Denver, Colorado, USA.

The ketogenic diet (KD) is a high-fat, low carbohydrate diet that is used as a therapy for intractable epilepsy. However, the mechanism(s) by which the KD achieves neuroprotection and/or seizure control are not yet known. We sought to determine whether the KD improves mitochondrial redox status. Adolescent Sprague-Dawley rats (P28) were fed a KD or control diet for 3 weeks and ketosis was confirmed by plasma levels of beta-hydroxybutyrate (BHB). KD-fed rats showed a twofold increase in hippocampal mitochondrial GSH and GSH/GSSG ratios compared with control diet-fed rats. To determine whether elevated mitochondrial GSH was associated with increased de novo synthesis, the enzymatic activity of glutamate cysteine ligase (GCL) (the rate-limiting enzyme in GSH biosynthesis) and protein levels of the catalytic (GCLC) and modulatory (GCLM) subunits of GCL were analyzed. Increased GCL activity was observed in KD-fed rats, as well as up-regulated protein levels of GCL subunits. Reduced CoA (CoASH), an indicator of mitochondrial redox status, and lipoic acid, a thiol antioxidant, were also significantly increased in the hippocampus of KD-fed rats compared with controls. As GSH is a major mitochondrial antioxidant that protects mitochondrial DNA (mtDNA) against oxidative damage, we measured mitochondrial H2O2 production and H2O2-induced mtDNA damage. Isolated hippocampal mitochondria from KD-fed rats showed functional consequences consistent with the improvement of mitochondrial redox status i.e. decreased H2O2 production and mtDNA damage. Together, the results demonstrate that the KD up-regulates GSH biosynthesis, enhances mitochondrial antioxidant status, and protects mtDNA from oxidant-induced damage.

 

[wookster]

http://en.wikipedia.org/wiki/SHBG

SHBG levels appear to be controlled by a delicate balance of enhancing and inhibiting factors. Its level is decreased by high levels of insulin and insulin-like growth factor 1 (IGF-1). Also, high androgen levels decrease SHBG, while high estrogen and thyroxine levels increase it.

However, recent evidence suggests that it is the livers production of fats that reduces SHBG levels,[2][3] not any direct effect of insulin and specific genetic mechanisms have been found that do this.

Of course, the liver produces more fats with a high carbohydrate diet... :badmood:

http://www.healthopedia.com/triglycerides/

Triglycerides are a common form of fat found in both food and the body. They make up 95% of the fat in the foods a person eats. They're also found in blood plasma and along with cholesterol, they make up the plasma lipids. Triglycerides occur naturally in foods. The liver also makes them from carbohydrates when calories are eaten that are not needed right away. They are stored in the body's fat tissue. Certain hormones control the release of triglycerides from the body's fat tissue as more energy is needed between meals.

Higher insulin levels are also associated with water retention of the epidermal tissues :alien:

 

[wookster]

I like Dr. Pepper.

Well, I didn,t know it was making me old, bald, and feeble :shock:

http://www.belfasttelegraph.co.uk/news/ ... 45511.html

A new health scare has erupted over soft drinks amid evidence they may cause serious cell damage.

[...]

Concerns centre on the safety of E211, known as sodium benzoate, a preservative used for decades by the £74bn global carbonated drinks industry. Sodium benzoate derives from benzoic acid. It occurs naturally in berries, but is used in large quantities to prevent mould in soft drinks such as Sprite, Oasis and Dr Pepper. It is also added to pickles and sauces.

[...]



Now, an expert in ageing at Sheffield University, who has been working on sodium benzoate since publishing a research paper in 1999, has decided to speak out about another danger. Professor Peter Piper, a professor of molecular biology and biotechnology, tested the impact of sodium benzoate on living yeast cells in his laboratory. What he found alarmed him: the benzoate was damaging an important area of DNA in the "power station" of cells known as the mitochondria.


He told The Independent on Sunday: "These chemicals have the ability to cause severe damage to DNA in the mitochondria to the point that they totally inactivate it: they knock it out altogether.


"The mitochondria consumes the oxygen to give you energy and if you damage it - as happens in a number if diseased states - then the cell starts to malfunction very seriously. And there is a whole array of diseases that are now being tied to damage to this DNA - Parkinson's and quite a lot of neuro-degenerative diseases, but above all the whole process of ageing."

 

[wookster]

:freaked: :freaked: :freaked:

http://www.hairloss-research.org/february1.html

First we must recognize that hair loss is the consequence of hair cell apoptosis, or programmed cell death. Apoptosis is the final result of what is termed the caspase activation cascade. Essentially DHT, superoxide, and other free radicals damage the cell’s mitochondria, and the damaged mitochondria in turn vomits cytochrome C, which activates the caspase 9 cascade. TGF-beta and alpha activate caspase 9 around hair follicles. The activated caspase 9 propagates downstream into caspase 3. Activation of caspase 3 is thought to be a direct cause of cell apoptosis (programmed cell death) in general.

Exactly how does DHT become toxic to scalp hair follicles and damge them? :dunno:


http://www.citeulike.org/user/jyuh/article/2827202

Apoptosis (programmed cell death) is a cellular self-destruction mechanism that is essential for a variety of biological events, such as developmental sculpturing, tissue homeostasis, and the removal of unwanted cells. Mitochondria play a crucial role in regulating cell death. Ca2+ has long been recognized as a participant in apoptotic pathways. Mitochondria are known to modulate and synchronize Ca2+ signaling. Massive accumulation of Ca2+ in the mitochondria leads to apoptosis. The Ca2+ dynamics of ER and mitochondria appear to be modulated by the Bcl-2 family proteins, key factors involved in apoptosis.

http://circres.ahajournals.org/cgi/cont ... l/97/4/302

Mitochondria are traditionally known as the energy generating centers of cells. Electron flux through the mitochondrial respiratory chain, an organized sequence of complex enzymes, hyperpolarizes the inner membrane, extruding newly generated ATP into the cytoplasm. An evolving paradigm shift has occurred in our understanding of mitochondrial function with the relatively recent observation that mitochondria are critical for the initiation of cellular apoptosis through release of cytochrome C.1 Mitochondria are also responsible for generation of substantial amounts of superoxide caused by electron leakage from the oxidative phosphorylation pathway. Reactive oxygen species (ROS) generated from mitochondria have been implicated in various forms of cell signaling in the vasculature.2

[...]

The discovery that mitochondrial function extends beyond ATP generation and that ROS may be key mediators of cellular physiology and pathology has opened new research vistas in vascular biology. Because mitochondria are responsible for the majority of ROS generated in most cells,11 linking mitochondrial respiration with ROS effects on cellular function is logical. Indeed excess release of mitochondrial oxidants has been implicated in the etiology of a host of pathologies including Alzheimer disease,12 degenerative changes in aging,13 Parkinson Disease,14 and type 2 diabetes.15

http://www.forhair.com/hair_growth.htm

Presumably, dihydrotestosterone inhibits energy production by keeping phosphodiesterase relatively inactive and by suppressing various protein (enzyme) synthetases. A relatively high concentration of cAMP may cause premature termination of the growing stages of hair follicles. Repetition of such processes over several years presumably transforms terminal follicles to vellus- type follicles and ultimately causes baldness. The diverse biologic effects of cAMP are mediated through activation of a family of protein kinases, which consist of a regulatory (R) and a catalytic (C) subunit; and when bound, these kinases are not active. Cyclic AMP binds to the R subunit, (a binding protein) for cAMP and subsequently releases the C subunit to form an active enzyme. Therefore, the more cAMP available in the androgen-sensitive hair follicles, the stronger the activation of the protein kinase. An increase in cAMP concentrations in hair follicles would produce diverse effects on various enzymes and reaction pathways. Inhibition of glycolysis - by the action of the active C subunit on the enzyme phosphofructokinase - decreases the energy available for the cell to maintain its metabolic functions. The same active subunit effectively slows posttranslational protein
synthesis and interferes with cell cycles at the C1 and S phases.36 These combined effects of high cAMP concentrations could result in premature completion of the anagen stage; and this, in turn, could yield follicles that are thinner and shorter than those of normal terminal hair.

http://en.wikipedia.org/wiki/Cyclic_ade ... ophosphate

Cyclic adenosine monophosphate (cAMP, cyclic AMP or 3'-5'-cyclic adenosine monophosphate) is a second messenger that is important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms.

:dunno: :lost: :dunno:

 

[FreeloaderUK]

brain overload!

 

[purecontrol]

Higher than optimal glucose and inslulin levels will cause #1inflamation #2higher androgen #3higher cortisol levels #4higher sensativity to androgen #5less capillaries = less circulation etc

androgens = test, dht, andros, etc

 

[wookster]

The explorer Vilhjalmur Stefansson appeared to be very healthy and very hairy on a low carb diet:

http://en.wikipedia.org/wiki/Vilhjalmur_Stefansson

Low-carb diet of meat and fish
Stefansson is also a figure of considerable interest in dietary circles, especially those with an interest in very low-carbohydrate diets. Stefansson documented the fact that most Inuit lived on a diet of about 90% meat and fish, often going 6-9 months a year on nothing but meat and fish--essentially, a no-carbohydrate diet. He found that he and his fellow European-descent explorers were also perfectly healthy on such a diet. When medical authorities questioned him on this, he and a fellow explorer agreed to undertake a study under the auspices of the Journal of the American Medical Association to demonstrate that they could eat a 100% meat diet in a closely-observed laboratory setting for the first several weeks, with paid observers for the rest of an entire year. The results were published in the Journal of the AMA, and both men were perfectly healthy on such a diet, without vitamin supplementation or anything else in their diet except meat.[6] However, hunters like the Inuits, who traditionally obtain most of their dietary energy from wild animals and therefore eat a low-carbohydrate diet,[7] seem to have a high mortality from stroke.[8]

 

[wookster]

http://en.wikipedia.org/wiki/Cyclic_ade ... ophosphate

Cyclic adenosine monophosphate (cAMP, cyclic AMP or 3'-5'-cyclic adenosine monophosphate) is a second messenger that is important in many biological processes. cAMP is derived from adenosine triphosphate (ATP) and used for intracellular signal transduction in many different organisms.

:dunno: :lost: :dunno:

Functions
cAMP is a second messenger, used for intracellular signal transduction, such as transferring the effects of hormones like glucagon and adrenaline, which cannot get through the cell membrane. Its purposes include the activation of protein kinases and regulating the effects of adrenaline and glucagon. It is also used to regulate the passage of Ca2+ through ion channels.

Calcium appears to be associated with negative consequences for anagen hair growth and potassium appears to be associated with beneficial effects that helps to extend the anagen phase of hair growth? Of course that probably has nothing to do with dietary intakes of calcium or potassium :bravo:

 

[wookster]

http://ajpcell.physiology.org/cgi/conte ... 287/4/C817

The mitochondrion is at the core of cellular energy metabolism, being the site of most ATP generation. Calcium is a key regulator of mitochondrial function and acts at several levels within the organelle to stimulate ATP synthesis. However, the dysregulation of mitochondrial Ca2+ homeostasis is now recognized to play a key role in several pathologies. For example, mitochondrial matrix Ca2+ overload can lead to enhanced generation of reactive oxygen species, triggering of the permeability transition pore, and cytochrome c release, leading to apoptosis. Despite progress regarding the independent roles of both Ca2+ and mitochondrial dysfunction in disease, the molecular mechanisms by which Ca2+ can elicit mitochondrial dysfunction remain elusive. This review highlights the delicate balance between the positive and negative effects of Ca2+ and the signaling events that perturb this balance. Overall, a "two-hit" hypothesis is developed, in which Ca2+ plus another pathological stimulus can bring about mitochondrial dysfunction.

 

[wookster]

I am guessing that potassium channel openers somehow prevent the Ca2+ overload associated with cellular apoptosis. :beer:

 

[wookster]

http://dsc.discovery.com/news/2008/08/1 ... cells.html

Aging Process Halted in Mouse Liver
ABC Science Online/AFP

Aug. 11, 2008 -- Scientists have stopped the aging process in an entire organ for the first time, a study released today says.

Published in today's online edition of Nature Medicine, researchers at the Albert Einstein College of Medicine at Yeshiva University in New York City also say the older organs function as well as they did when the host animal was younger.

The researchers, led by Associate Professor Ana Maria Cuervo, blocked the ageing process in mice livers by stopping the build-up of harmful proteins inside the organ's cells.

As people age, their cells become less efficient at getting rid of damaged protein resulting in a build-up of toxic material that is especially pronounced in Alzheimer's, Parkinson's and other neurodegenerative disorders. The findings suggest that therapies for boosting protein clearance might help stave off some of the declines in function that accompanies old age.

In experiments, livers in genetically modified mice 22 to 26 months old, the equivalent of octogenarians in human years, cleaned blood as efficiently as those in animals a quarter their age.

By contrast, the livers of normal mice in a control group began to fail.

The benefits of restoring the cleaning mechanisms found inside all cells could extend far beyond a single organ, said Cuervo.

"Our findings are particularly relevant for neurodegenerative disorders such as Parkinson's and Alzheimer's," she said. "Many of these diseases are due to 'misbehaving' or damaged proteins that accumulate in neurons. By preventing this decline in protein clearance, we may be able to keep these people free of symptoms for a longer time."

If the body's ability to dispose of cell debris within the cell were enhanced across a wider range of tissues, it could extend life as well. In healthy organisms, a surveillance system inside cells called chaperone-mediated autophagy (CMA) locates, digests and destroys damaged proteins.

Specialized molecules, the "chaperones," ferry the harmful material to membrane-bound sacs of enzymes within the cells known as lysosomes. Once the cargo has been "docked," a receptor molecule transfers the protein into the sac, where it is rapidly digested.

With age, these receptors stop working as well, resulting in a dangerous build-up of faulty proteins that has been linked, in the liver, to insulin resistance as well as the inability to metabolize sugar, fats or alcohol.

The same breakdown of the cell's cleaning machinery can also impair the liver's ability to remove the toxic build-up of drugs at a stage in life when medication is often part of daily diet.

In genetically modified mice, Cuervo compensated for the loss of the receptors in the animals by adding extra copies.

"That was enough to maintain a clean liver and to prove that if you keep your cells clean they work better," she said.

The study goes a long way towards settling a sharp debate in the field of ageing research. Leading Australian ageing researcher David le Couteur, Professor of Geriatric Medicine at the University of Sydney, says the paper is a major breakthrough.

"She has single-handedly shown that lysosome function is a crucial part of the ageing process," he said.

He added, Cuervo has also shown the critical role the lysosomal receptor molecules play in keeping the liver clean of damaged proteins.

While her paper does not show increased survival rates among the mice, le Couteur, who has advised her recently on the research, says Cuervo does have data on improved survival rates which she intends to publish.

Cuervo is now working with pharmaceutical companies to identify drugs that will turn the receptors on, or make them more active. She believes maintaining efficient protein clearance may improve longevity and function in all the body's tissues.

It is also possible that the same kind of "cellular clearance" can be achieved through diet, she said. Research over the past decade has shown that restricted calorie intake in animals, including mammals, significantly enhances longevity.

"My ideal intervention in the future would be a better diet rather than a pill," she said.

 

[wookster]

http://circ.ahajournals.org/cgi/content ... 13/13/1675

Background— Studies suggest that magnesium intake may be inversely related to risk of hypertension and type 2 diabetes mellitus and that higher intake of magnesium may decrease blood triglycerides and increase high-density lipoprotein (HDL) cholesterol levels. However, the longitudinal association of magnesium intake and incidence of metabolic syndrome has not been investigated.

Methods and Results— We prospectively examined the relations between magnesium intake and incident metabolic syndrome and its components among 4637 Americans, aged 18 to 30 years, who were free from metabolic syndrome and diabetes at baseline. Metabolic syndrome was diagnosed according to the National Cholesterol Education Program/Adult Treatment Panel III definition. Diet was assessed by an interviewer-administered quantitative food frequency questionnaire, and magnesium intake was derived from the nutrient database developed by the Minnesota Nutrition Coordinating Center. During the 15 years of follow-up, 608 incident cases of the metabolic syndrome were identified. Magnesium intake was inversely associated with incidence of metabolic syndrome after adjustment for major lifestyle and dietary variables and baseline status of each component of the metabolic syndrome. Compared with those in the lowest quartile of magnesium intake, multivariable-adjusted hazard ratio of metabolic syndrome for participants in the highest quartile was 0.69 (95% confidence interval [CI], 0.52 to 0.91; P for trend <0.01). The inverse associations were not materially modified by gender and race. Magnesium intake was also inversely related to individual component of the metabolic syndrome and fasting insulin levels.

Conclusions— Our findings suggest that young adults with higher magnesium intake have lower risk of development of metabolic syndrome.

 

[wookster]

True? False? :dunno:

http://www.nourishingperspectives.com/p ... _diet.html

High Protein Diet and Prostate Enlargement


A high protein diet has been shown to inhibit 5-alpha-reductase which may result in a reduction of the conversion of testosterone to DHT, a more potent form of testosterone, which has been implicated in prostate enlargement.



Conversely a low protein, high carbohydrate diet stimulates 5-alpha-reductase.

http://www.enlargedprostateremedy.com/h ... d-prostate

healthy eating plan is one of the cornerstones of a healthy prostate. Follow these nutritional guidelines to keep your prostate in good shape:

Follow a low fat / high protein diet. Aim to get about 45% of your calories from protein a high protein diet may inhibit the production of 5-alpha-reductase, the enzyme that converts testosterone to DHT).

Keep your carbohydrates to about 35% of your total calories.

Consume plenty of essential fatty acids.

Look for whole, unprocessed foods and eat plenty of sunflower or pumpkin seeds each day.

Drink plenty op fluids

Increase your fiber intake

Include soy in your diet.

 

[wookster]

Low Carb Diet May Stunt Prostate Tumor Growth

Mice fed no-carb diet had smaller tumor volumes and prolonged survival relative to mice fed other diets

http://www.prostatecancerfoundation...Carb_Diet_May_Stunt_Prostate_Tumor_Growth.htm

Low Carb Diet May Stunt Prostate Tumor Growth

Mice fed no-carb diet had smaller tumor volumes and prolonged survival relative to mice fed other diets

By Joene Hendry

Thursday, November 22 (Reuters Health) - A study conducted in mice suggests a potential link between carbohydrate intake and prostate tumor growth. In the study, researchers observed significantly less tumor growth in mice fed a no-carbohydrate diet compared to those fed a Western-style diet.

"There is a link between diet and prostate cancer," Dr. Stephen J. Freedland of Duke University Medical Center, Durham, North Carolina, told Reuters Health. "What exactly that link is and how best to use it to prevent and treat prostate cancer remains unclear."

Recent studies have suggested that carbohydrate intake may influence prostate cancer biology, Freedland and colleagues note in a report in the journal Prostate. To investigate further, they compared prostate tumor growth in 75 mice equally separated into three diet groups.

The no-carb diet provided zero percent carbohydrates and 84 percent fat; the low-fat diet provided 72 percent carbohydrate and 12 percent fat; and the Western diet provided 44 percent carbohydrate and 40 percent fat. All three diets provided 16 percent of the total calories as protein.

The researchers found that mice fed a no-carb diet had tumor volumes up to 33 percent smaller, on average, than mice fed the Western-style diet. Average tumor volumes did not differ significantly between mice eating the low-fat or Western diets.

Mice fed the no-carb diet also had significantly prolonged survival relative to mice fed the Western diet.

The researchers observed that the no-carb diet was associated with a reduction in serum insulin and insulin-like growth factor type 1 (IGF-1) -- a protein that helps spur cells to multiply and has been implicated in the cancer process -- and with an increase in a related protein called IGF-BP3, which blocks the action of IGF-1.

Within a year, the investigators hope to assess how following a low carbohydrate diet for one month prior to prostate cancer surgery might impact tumor growth in men.

But Freedland cautions that clinical trials, such as this, need to replicate animal study findings before any general claims concerning carbohydrate intake and prostate tumor growth can be made in humans.

SOURCE: The Prostate online edition, November 13, 2007

 

[propaganda]

From my own experience going high protein-fat, low carb gave me boost in energy and overall better feeling. Dunno about hair. Veggie diet made me weak so im not going back to that route again.

 

[wookster]

:hairy: :hairy: :hairy:

http://www.helium.com/debates/80363-can-low-carb-diets-help-reducing-acne/side_by_side?page=1

In the past few years, the issue of carbohydrates and acne has returned to the attention of scientists, thanks to the works of Cordain and colleagues (2002, 2003, 2005), which demonstrated that high sugar intake (i.e. high "glycemic load") can induce hormonal changes that are commonly associated with acne, namely high peaks of insulin release that consequently stimulate an increase in blood levels of androgens and IGF-1. The implication of insulin in acne is further suggested by the high prevalence of acne in women suffering from polycystic ovary syndrome, a disease characterized by high insulin and androgen levels (Franks, 2003).

The most significant evidence of a link between carbohydrates and acne has been provided very recently by the research of dr. Smith and colleagues from RMIT University of Melbourne, Australia. In 2007, they recruited 43 young men with acne, which they randomly assigned to a low-carb diet versus a high-carb diet. After 3 months, they observed a significant reduction in the number and severity of skin lesions in the first group, compared with the second group. Moreover, the low-carbohydrate diet was associated with a decrease in blood levels of androgens and IGF-1, which could be the key effect of this kind of diet. The findings of the Australian team are most interesting; however, further research to confirm these results is expected from others, as well.