It must be converted from folic acid to methyltetrahydrofolate (5-MTHF) before it can be used by the body.

The big variations in how efficiently folic acid reaches the target organs depend from 2 different points:

1. Gut absorption

2. Liver conversion of FA in the active form

Unmetabolized Folic Acid (UMFA) may be found in the circulation at doses of supplementation of FA > 200μg in normal subjects.

The human gut appears to have a very efficient capacity to convert reduced dietary folates to 5-MTHF but limited ability to reduce folic acid.

Methyltetrahydrofolate Reductase(MTHFR) :

Rate-limiting enzyme that catalyzes the irreversible conversion to 5-MTHF in the methyl cycle

10% of the world’s population is affected by homozygous (TT) MTHFR polymorphism

Particularly common in some ethnic groups, northern China (20%), southern Italy (26%), and Mexico (32%)

Most common uses of folate / Quatrefolic® Folates application areas :

Neural-tube Defects Irritable bowel disease

Male and female infertility Cognitive impairment in elderly

Spontaneous abortion

Lifestyle putting people at risk of low folate levels:

Smoking

Alcohol

excess Eating disorders

Low vegetables intake

Chronic dieting

Coronary heart disease

Epilepsy

Macrocytic anemia

Mood

Elevated homocysteine levels

MTHFR SNPS

Not long ago, this molecule was only known for its activity as an intermediate in nicotinamide adenine dinucleotide (NAD+) biosynthesis.

Recently, preclinical studies have demonstrated diversified pharmacological activities of NMN in cardiac and cerebral ischemia, Alzheimer’s disease, diet- and age-induced type 2 diabetes, and obesity, all of which are linked up to the deficiency of NAD+ [6,7,8]. Camacho-Pereira et al. have shown that an increased level of NAD+ consuming enzymes e.g., NAD+ dependent acetylase (Sirtuins), poly ADP-ribose polymerase (PARP), NADase (CD38) contribute to the decline of NAD+ with age [9]. In mammalian cells, CD38, a type of cell surface NADase enzyme, causes breakdown of NAD+ to form nicotinamide and (cyclic-)ADP-ribose [10]. On the other hand, expenditure of NAD+ helps PARP to produce branched ADP-ribose polymers that help in DNA repairing. Another group of NAD+ consuming enzymes, sirtuins (SIRT 1-7) performs different functions by consuming NAD+. Apart from deacetylation, which is the most common NAD+ mediated function of sirtuins, other functions like desuccinylase, demalonylase, lipoamidase, and deglutarylase enzymatic activity are noteworthy that help in the cellular adaptation of energy deficit and improvement of metabolic function. Administration of NMN can compensate for the deficiency of NAD+ caused by these NAD+ consuming enzymes.

NMN shares similar properties like other NAD+ precursors- nicotinamide riboside (NR), nicotinic acid, and nicotinamide. Unlike NMN, nicotinic acid, and nicotinamide have several disadvantages in terms of their therapeutic application. Nicotinamide may cause hepatotoxicity or flushing, while a recent preclinical study suggests that it resides in the rat body for a shorter period of time compared to NMN. Niacin or nicotinic acid is associated with adverse effects like cutaneous flushing when administered as an immediate release formulation whereas the sustained release formulations may cause hepatotoxicity. Among the NAD+ precursors, NR and NMN are exceptions as fewer unfavorable side effects have been reported for these two metabolites. Moreover, nicotinamide riboside is also orally bioavailable like NMN. Considering these, NMN could be proposed as a preferable therapeutic option that can be supported by several ongoing clinical trials.

NAD+ is synthesized by three different pathways in mammalian cells-

1. de novo pathway-synthesis from tryptophan,
2. salvage pathway-synthesis from either nicotinamide or nicotinic acid, or
3. conversion of NR

Biosynthetic pathway of nicotinamide mononucleotide in mammalian cells.

References :
1. Bieganowski P., Brenner C. Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans. Cell. 2004;117:495–502. doi: 10.1016/S0092-8674(04)00416-7. [PubMed] [CrossRef] [Google Scholar]
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Cellular Activation : The fundamental problem (not allowing brain cells to produce dopamine in Parkinson’s disease) is a deficiency in the energetics of these cells. L-dopa has been shown to lead to further compromise of the brain’s ability to produce energy. This reduces further the brain’s ability to produce dopamine.

NADH (Nicotinamide Adenine Dinucleotide) : Study of 885 patients who received NADH showed an 80% moderate to excellent improvement in their disability.

Coenzyme Q-10 :  Parkinson’s patients have a deficiency of coenzyme Q-10. This may be why they produce an inadequate supply of dopamine. Coenzyme Q-10 levels correlate with the activities of complexes I and II/III in the mitochondria. Ubiquinol is 8x better absorbed and more effective than the ubiquinone form. Statin drugs lower dramatically serum coenzyme Q-10 levels. 100-120 mg a day of coenzyme Q-10 supplementation is suggested to patients on a statin drug. Large dosages of coenzyme Q-10 have been used to treat Parkinson’s Disease (300 mg-1,200 mg a day). High dosages should only be used under the direction of a physician since larger amounts of coenzyme Q-10 on a daily basis may have side effects.

Phosphatidylserine :  Is one of the key components of neuronal membranes. Phosphatidylserine may enhance the effectiveness of what little dopamine remains. Dosage: 300 mg a day. No known side effects.

Antioxidant Protection :  Important role in protecting the brain from free radical damage. Research goes back to 1988 when a case controlled study revealed those who consumed diets rich in nuts had a risk of Parkinson’s disease only 39% of controls. Consumption of plums was associated with a risk reduced to 24% of the average population. Vitamins E and C were given to a large group of Parkinson’s patients over several years.Initially, none of the patients needed L-dopa. The time until patients required L-dopa therapy was extended 2.2 years in those taking vitamin E and C.

Vitamin E :  Use only natural vitamin E (d-alpha tocopherol), not dl-alpha tocopherol since the latter is synthetic and less biologically active.

N-acetyl-cysteine (NAC) :  Glutathione is easily digested to is constituent amino acids, and before we couldnot administer by mouth…now we have S-acetyl-glutathione well absorbed orally) but also NAC directly encourages brain glutathione production and it can be given by mouth. This activity is increased in the presence of adequate vitamin C and E. NAC is itself a potent antioxidant by reducing the formation of nitric oxide which has been implicated as have a role in the cause of Parkinson’s disease.

Acetyl-L-carnitine :  Like coenzyme Q-10 and NADH, acetyl-L-carnitine increases energy production in damaged neurons. Study reported in 1995, researchers demonstrated the ability of acetyl-L-carnitine to completely prevent parkinsonism in laboratory animals.

Alpha Lipoic Acid :  Is an antioxidant, also serves as a metal chelator, metals can increase the formation of free radicals, Parkinson’s patients have an increased concentration of iron in their brains.

Vitamin D : High prevalence of vitamin D deficiency and reduced bone mass in Parkinson’s disease sufferers.

Ginkgo Biloba :  Has brain antioxidant activity, protects the brain against neurotoxins, very useful in Parkinson’s disease in those exposed to herbicides and other chemical agents.

Vitamin C :  Vitamin C helps to preserve the energy producing capacity of the mitochondria which is an abnormality made worse by the administration of L-dopa.

DHEA :  The body’s master hormone that regulates other hormones tends to be low in parkinson’s disease sufferers and should be checked and replenished.

Hyperbaric oxygen and infra-red saunas and ozone therapies are other treatment modalities I would entertain

Several studies have also observed that the gut microbiome is markedly altered in patients with Parkinson’s disease and that faecal microbiota transplantation can have a protective effect in animal models of Parkinson’s. The reason for this is unknown; however, an interesting observation is that another common pathology seen in Parkinson’s disease is the accumulation of misfolded α-synuclein proteins, called Lewy bodies, in the brain.

It has been shown that certain sensory cells of the gut contain α-synuclein. Researchers have hypothesised that it is possible that abnormal forms of the α-synuclein protein could travel from the gut to the brain through the vagus nerve, a phenomenon that has been shown in animal models of Parkinson’s. Further support for this theory comes from findings that people who have had a surgical vagotomy — where branches of the nerve are cut — have a lower lifetime risk of developing Parkinson’s.

“We know that infrared light can reduce Parkinson’s symptoms and offer protection to brain cells. So, we wanted to test if it could modulate the gut’s microbiome as well,” Liebert said.
One of the principal researchers in Liebert’s planned study, Dr Daniel Johnstone, scientist and lecturer at The University of Sydney’s Bosch Institute, had previously undertaken a study showing that exposure to infrared light altered the gut microbiome in mice. “The ability of PBM [light therapy] to influence the microbiome (if proven to be applicable to humans) will allow an additional therapeutic route to target multiple diseases, including cardiovascular disease and Parkinson’s disease, many of which have thus far eluded effective treatment approaches,” the paper concludes.

Kiat is excited by light therapy’s potential. “If we can create non-invasively a metabolically healthier microbiome through this extremely cheap and easy way, then inflammatory diseases and neurodegenerative diseases should be positively influenced,” he said.

References

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3. Study giving Parkinson’s patients IV glutathione BID for 30 days Results: All patients improved significantly after glutathione therapy, with a 42% decline in disability. Once glutathione was discontinued, the therapeutic effect lasted 2-4 months. Study also found that glutathione possibly retards the progression of the disease. Sechi, G., et al., “Reduced glutathione in the treatment of early Parkinson’s disease,” Prog Neuropsychopharmacol Biol Psychiatry 1996; 20(7):1159-70.
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Cholesterol is in every cell of the body, where it helps produce cell membranes, steroid hormones, including sex hormones, vitamin d and bile acids that are needed to digest fat. Cholesterol also helps in the formation of new memories and is vital for the formation of new memories and is vital for normal neurological functioning.

The liver produces about 75% of your body’s cholesterol (1).

The American heart association recommends that your total cholesterol and ldl be kept below a certain level (and these guidelines are constantly being aggressively modified to lower your cholesterol even more). However total cholesterol is not a good predictor of heart disease unless extremely high.

What about other ratios that are better predictors of heart disease :

1. total cholesterol/hdl ratio <4 is optimal Each drop in 1 equates to a 60%change in risk, ie a value of 6 = 120% increased risk, a value of 3 a 60% reduction in risk
2. b)Triglyceride/hdl ratio – This should be below 2

HDL (good cholesterol) is a very potent heart disease risk factor.  Why do we concentrate too much on total cholesterol and ldl levels when high levels of these aren’t always associated with heart disease (if your inflammation and oxidative stress are low)? Shouldn’t we be looking at ways to lower inflammation and oxidative stress and look at ALL the cardiovascular risk factors?    One might say there is good ldl and bad ldl (inflamed oxideised ldl)

Remember cholesterol is not the only player in the risk of heart disease.    There are many risk factors :

Oxidation refers to the process of some material combining with oxygen, either in the air or in the body. Fats that have become oxidized are referred to as being rancid. The process begins with damage to the inner lining of the blood vessels. Cells is the arterial wall begin to pick up oxidized lipoprotein from the blood (like oxidized ldl). Other materials such as cholesterol esters, calcium, fibrinogen, and other fatty materials, become incorporated in the build up of atheromas. This accumulation of oxidized fats can occur only if tissue levels of antioxidants (Vit A, E, C, Superoxide dismuatase are depleted)

Prevent arterial “rust” references 25-32

Summary of Nutrition Guidelines for Dyslipidemia Treatment :

1. Mediterranean and paleo diets are recommended.
2. Reduce saturated fats to about 10% of total fat intake.
3. Eliminate trans fats.
4. Increase monounsaturated fats to 40% of total fat intake.
5. Increase polyunsaturated fats (ω-3 fats) to 40%-50% of total fat intake.
6. Increase viscous fiber to 50 g/d.
7. Increase vegetables to 6 servings per day.
8. Increase fruits to 4 servings per day.
9. Add plant sterols and nuts to diet.
10. Reduce refined carbohydrates and use low glycemic foods. Use more complex carbohydrates.
11. Consume high quality protein with cold water fish and organic lean meat and poultry.
12. Maintain ideal body weight and body composition.

Nutraceutical supplementation and heart health :

References :
1. American heart associationjanuary 23, 2008 http://www.americanheart.org/presenter.jhtml?identifier=3046105
2. Mercola.com, Cholesterol is NOT the cause of heart disease, Ron Rosedale May 28,2005 http://www.mercola.com/2005/may/28/cholesterol_heart.htm
3. Fallon,S. and Mary Enig. “Dangers of statin drugs : What you haven’t been told about popular cholesterol lowering medicines,” The Weston A. Price Foundation http://www.westonaprice.org/moderndiseases/statin.html
4. Pyscosomatic medicine 2000;62 http://articles.mercola.com/sites/articles/archive/2000/03/26/cholesterol-depression.aspx
5. Epidemiology 2001 Mar; 12 168-172 http://articles.mercola.com/sites/articles/archive/2001/08/08/suicide.aspx
6. Annals of Internal Medicine (1998;128(6):478-487 The journal of the American medical association (1997;278:313-321) http://articles.mercola.com/sites/articles/archive/2008/01/02/low-cholesterol-linked-to-violence.aspx
7.The journal of the American College of Cardiology July 31,2007;50:409-418http://content.onlinejacc.org/cgi/content/short/50/5/409
8. Annals of internal medicine October 3,2006; 145(7): 520-530 http://www.annals.org/cgi/content/full/145/7/520
9. USA Today.com October 16,2004 http://www.usatoday.com/news/health/2004-10-16-panel-conflict-of-interest_x.htm
10. American heart association, “what your cholesterol level means,” accessed May 22,2008 http://www.americanheartorg/presenter.jhtml?identifier=183
11. MSNBC.com More than half of Americans on chronic meds May 14,2008 http ://www.msnbc.msn.com/id/24603120 (accessed June 9,2008)
12. Businessweek Do cholesterol drugs do any good ? January 17,2008 http://www.businessweek.com/magazine/content/08_04/b4068052092994.htm (accessed June 9, 2008)
13. The journal of clinical investigation December 2007;117(12): 3940-51 http://www.ncbi.nim.nih.gov/sites/entrez?orig db=Pubmed&cmd=Search&TransSch ema=title&term=%22The%20Journal%20investigation%22%5BJour%5D%20A ND%202007%2F12%5Bpdat%5D%20AND%20atroqin-1
14. Mercola.com Sudden memory loss linked to cholesterol drugs http://articles.mercola.com/sites/articles/archive/2003/07/30/cholesterol-drugs-part-six.aspx
15.Nature Medicine September,2000;6:965-966,1004-1010. http://articles.mercola.com/sites/articles/archive/2000/09/10/statins-cancer.aspx
16. Nature medicine, december,2000;6:1311-1312,1399-1402 http://articles.mercola.com/sites/articles/archive/2000/12/24/statins-part-two.aspx
17. Edwards, I Ralph; Star, Kristina; kuru, Anne, “statins, neuromuscular degenerative disease and an amyotrophic lateral sclerosis-like syndrome,” Drug safety, volume 30, number 6,2007, pp.515-525(11) http://www.ingentaconnect.com/content/adis/dsf/2007/00000030/00000006/art0005
18. IMS Health.IMS National Prescription audit Plus July 2007. http:www.lipitor.com/
19. BusinessWeek.com, “Do cholesterol drugs do any good?” January 17,2008-09-01 http:www.businessweek.com/magazine/content/08_04/b4068052092994.htm (accessedJune 10, 2008)
20. New York Times, “cardiologists question delay of data on 2 drugs,” November 21,2007 http://www.nytimes.com/2007/11/21/business/21drug.html? r=2&ex=1353387600&en=db5fb1664 6a23bbd&ei=5088&partner=rssnyt&emc=rss&oref=slogin&oref=slogin (accessed June 10,2008)
21. New York times, “drug has no benefit in trial, markers say,” January 14,2008 http://www.nytimes.com/2008/01/14/business/14cnd-drug.html?ex=1357966800&en=181407fac186f36a&ei=5088&partner=rssnyt&emc=rss (accessed June 10,2008)
22. Enig, Mand Sally Fallon, “the skinny of fats,” the Weston A.PriceFoundation, http://www.westonaprice.org/knowyourfats/skinny.html||10
23. lackland, D T, et al, j Nutr, Nov 1990, 120: 11S : 1433-1436
24. Nutr week, mar 22,1991,21:12:2-3
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26. Cathcart, M.K.,et al Journal of of leukocyte biology 1985; 38:341-350
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Fisetin a plant flavonoid found in fruits mostly in strawberries appears about as effective in mice as any of the current top senolytics, such as the chemotherapeutics, dasatinib, and navitoclax. Per the research data, dosing with fisetin destroys 25% -50% of senescent cells depending on organ and method of measurement.  The dose level is large in absolute terms, as one might expect for a flavonoid. For aged mice and a one-time treatment, the researchers used 100 mg/kg daily for five days! The usual approach to scale up estimated doses from mouse studies to initial human trials leads to 500 mg per day for five days for a 60kg human.

DOSAGE: That’s around 750 mgs per day with 1gm a day of Quercetin for 7 days ‘while fasting’ to eliminate 25-50% of senescent cells from a 180lb human. This is a one week program that should be done once every 6 months or so.

Quercetin

Quercetin is a flavonol pigment found in fruits and vegetables; its highest concentration is found in capers. Quercetin has antioxidant properties that work to protect the body from free radicals and oxidative stress! Quercetin is a more powerful antioxidant than vitamin C, vitamin E, or beta carotene! Quercetin may contain anticancer properties that might help prevent the spread of cancerous cells and tumor growth.

A 2015 report found that quercetin restricted the growth of prostate cancer cells in mice and rats. A 2018 in vitro study indicated that quercetin showed promise in both the treatment and prevention of prostate cancer. There are other benefits you can research further yourself.

DOSAGE: The most common dose is 500 mg per day for regular therapeutic maintenance use, but, for senescent removal program a 1gm per day of Quercetin in combination with Fisetin 750 mgs a day (as replacement for dasatinib) for 7 days ‘while fasting’ for removal of senescent cells from the body.

This is a one week program that should be done once every 6 months or so.

Resveratrol as an everyday maintenance program against senescent cells, Resveratrol, a known activator of SIRT1 which slows aging, and has been demonstrated to inhibit mTOR activity and cellular senescence!

DOSAGE: 1gm a day in the mornings when intermittent fasting or longer fasts to inhibit mTOR, to promote autophagy is desired

However, as with autophagy and mTOR – too much or too little of anything is bad as having either too low or too high levels of IGF-1 increases risk of mortality. IGF-1 as well as mTOR help to deal with environmental stressors by supporting repair processes and anabolic growth!

High circulating IGF-1 levels are associated with longer telomere length, which predicts longer life!

1) IGF-1 prevents age-related cognitive decline by promoting neurogenesis in rats.

2) IGF-1 deficiencies cause sarcopenia and muscle wasting.

3) IGF-1 increases glutathione peroxidase, which is one of the main antioxidant pathways in the body.

4) IGF-1 fights autoimmune disorders and lowers inflammation by promoting anti-inflammatory T Regulatory Cells.

Although the link between mTOR mediated IGF-1 and accelerated aging is not very strong, you’d still not want to be anabolic and growing 24/7. It’s an evolutionary mismatch as no living organism in nature would get access to high amounts of growth promoting fuel all the time.

HOW TO INCREASE AUTOPHAGY

The most effective and easiest way to promote autophagy is to do intermittent fasting!       This and caloric restriction are one of the few ways we know how to increase lifespan in all species!

1) You should fast for at least 16 hours every day to even enter a fasted state! To really activate autophagy you’d have to fast for longer than that but you don’t want to have too much autophagy every day! That’s why daily time-restricted feeding with 16/8, 18/6, 20/4 or one meal a day is very good for keeping cellular turnover active throughout the days!

2) Control your insulin and blood sugar levels! Carbohydrates and amino acids from protein are going to suppress autophagy directly by stimulating insulin, IGF-1, and mTOR. That’s why a high carb nor a high protein diet alone is ideal for longevity! They do help with building muscle and strength but you don’t want to be anabolic all the time! It’s a good idea to spike anabolism only during certain parts of the day and only briefly!

3) Caloric restriction and methionine restriction can promote life extension by decreasing mTOR activity! I’d say whatever the diet is the main reasons for increased lifespan have to do with being in a state of energy deprivation under which AMPK gets elevated and thus promoting autophagy to some extent! To reap the full benefits of autophagy you’d have to be strictly fasting but you can experience milder autophagy with carb restriction and protein restriction!

4) Exercise can also stimulate autophagy! However, you’d have to do it in a state of glycogen depletion wherein you’ve activated AMPK. This can be achieved through carbohydrate restriction or exercising in a fasted state! The best time to consume calories is in a post-workout setting because you’ll be tapping into autophagy during exercise and then the food you eat later will be used primarily for lean muscle growth not fat storage nor accelerated aging!

5) Have extended fasts for 3-7 days a few times per year! This is necessary for tapping into a deeper state of autophagy that helps to rejuvenate old cells and promotes longevity! These extended fasts should be coupled with periods of higher anabolism and building muscle so that you could recover from the catabolic stressors!

That’s why the idea of intermittent fasting does not equal starvation or malnourishment. Even on the daily one meal a day schedule, you’ll be eating a lot of calories. You’ll simply be doing it within a restricted time frame and because of that you reap the benefits of both muscle growth and life extension! Timing is the most critical component to manipulating the Kinase Triad.

ADD THESE FOR AUTOPHAGY ONLY WHEN YOU DON’T WANT TO ACTIVATE mTOR

There are certain autophagy boosting foods that promote longevity! They also mimic the effects of exercise and fasting!

1) Rapamycin, is an antifungal agent that inhibits mTOR. It’s also known to suppress tumor growth and increase the lifespan in mice.

2) Sulforaphane, found in green leafy vegetables and highly concentrated in broccoli sprouts and cruciferous.

3) Curcumin, induces autophagy by activating AMPK. Piperine, which is a compound found in black pepper induces autophagy and it also boosts the bioavailability of Curcumin, which makes it a double whammy!

4) Medicinal mushrooms like chaga, reishi, shitake, and lion’s mane support autophagy and fight cancers.

5) 6-Shogaol, is a compound in ginger induces autophagy by inhibiting the AKT/mTOR pathway in human non-small cell lung cancer.

6) Resveratrol, inhibits breast cancer growth and has longevity-boosting effects because it turns on the Sirt1 DNA gene associated with longevity, also turned on when fasting!

7) The compound EGCG found in green tea induces autophagy.

8) Caloric restriction mimicking ingredients like Malabar tamarind (Hydroxycitrate), Berberine, Rapamycin trigger autophagy.

9) Polyphenols regulate autophagy. Polyphenols and Flavonoids are found in dark berries, dark leafy green vegetables, and all kinds of herbs and spices!

Why Infrared Light?

The optimum wavelength for max. skull penetration is between 805 nm and 830 nm (infrared). Studies show that the light reaches a depth of 4-5 cm.

LED therapy is non-invasive, painless and non-thermal.

Mechanisms of working :

a) Stimulation of the mitochondrial respiratory chain (cytochrome c oxidase)
b) Release of NO by photodissociation vasodilatory effects
c) Brief increase in reactive oxygen species
d) Improved oxygen availability and oxygen consumption
e) Activation of signaling pathways and transcription factors that cause long-lasting changes in protein expression
f) Increases ATP production

Over and above the mitochondrial effects listed above the transcranial low level laser also :

• Improves lymphatic flow = Increased cerebral blood flow
• The signaling pathways and activation of transcription factors lead to the eventual effects of PBM (photobiomodulation) in the brain
• Short-term stimulation: ATP, blood flow, lymphatic flow, cerebral oxygenation, less edema
• Neuroprotection: Upregulation of anti-apoptotic proteins, less excitotoxity, more antioxidants, less inflammation
• Processes that help the brain to repair itself: Neurotrophins, neurogenesis and synaptogenesis

References : available on request.

Because the gut is shaped throughout your life by things such as how much sleep and exercise one gets, levels of chronic stress, and of course, what food, drink and medications are ingested, the overall focus of Viome is lifestyle-based health care that can help with weight loss, sleep, mental clarity, digestive issues, your skin and more.

Viome is a gut microbiome sequencing test that can identify living microorganisms in one’s gut as well as determine what these organisms are producing and whether or not it is causing the body harm. Based on this, scores are received that provide a clear picture of how what you eat  positively, or negatively, contributes to the health of the gut microbiome and what can be done to improve it.

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Phosphatidylcholine focus:

Phosphatidylcholine (PC) has also biological and functional roles in healthy liver. It is one of the most important support nutrients for the liver, a large biological molecule that is a universal building block for cell membranes. More than 2 decades of clinical trials indicate that PC protects the liver against damage from alcoholism, pharmaceuticals, pollutant substances, viruses, and other toxic influences, most of which operate by damaging cell membranes. Dietary supplementation with PC (a minimum 800 mg daily, with meals) significantly speeds recovery of the liver. PC is fully compatible with pharmaceuticals, and with other nutrients. PC is also highly bioavailable (about 90% of the administered amount is absorbed over 24 hours), and PC is an excellent emulsifier that enhances the bioavailability of nutrients with which it is coadministered. (Kidd PM. Phosphatidylcholine: A Superior Protectant Against Liver Damage. Alternative Med. Rev. 1996) PC’s diverse benefits and proven safety indicate that it is a premier liver nutrient:

• It is the principal molecular building block for circulating lipoproteins
• It is an important emulsifier in the lungs gastrointestinal tract bile
• It manages the vast majority of life processes
• It acts as a carrier for both fat-miscible and water-miscible nutrient

Uses and doses :

Phosphocomplex® is obtained by hydrogen bonds between the polar head of phospholipids and the polar groups of pure Silybin (≥ 95%). The standardized starting material is equal to ≥29% to ≤37% of Silybin by HPLC. The enhanced absorption through gastro-intestinal tract and the increased bioavailability facilitates liver targeting, with a synergistic effect of the phosphatidylcholine phospholipid as hepatoprotector. Supported by pharmacological and clinical data. Phosphocomplex ™ is a yellow-brownish powder suitable for different formulation such as tablets, capsules and sachets.

At the recommended dosage of 80 – 160 mg/day it may be indicated as a complement product for :

• Fatty Liver –Steatosis
• Alcoholic liver disease
• Also Non Alcoholic Fatty Liver Disease
• Chronic liver disease
• Acute viral hepatitis.

Mechanisms of working of phosphocomplex :

1. Hepatocye protection : promotes hepatocyte protein synthesis, a mechanism forliver cell regeneration

2. Anti-inflammatory effects
a) mastocytes stimulated
b) neutrophil stimulation
c) leucotrine inhibition
d) Prostaglandin, lipoprotein and lnterleucin inhibition

3. Detoxification : increases GSH, increases superoxide dismutase

4. Liver protection : stimulates the flow of bile acid and the production of bile salts, and protection of hepatic tissue