Quatrefolic The 4th Generation Folate

Quatrefolic The 4th Generation Folate

Folate plays an essential role in cell division and DNA synthesis and is involved in human growth and development. Humans need to maintain an adequate dietary intake of folate during various stages of their lives.

Folates contained in foods are unstable and susceptible to oxidation and they lose activity during food processing, manufacturing and storage.

Bioavailability range of 25-50%, depending on the kind of food, Room temperature storage may lose up to 70% of their folate activity within three days, Cooking process in water can increase the loss to 95%.

Primary Folates :

Structurally-related compounds (as polyglutamated forms)

Naturally found in foods

Must be hydrolyzed Unstable (food processing and storage)

Secondary Folic :

Synthetic oxidized form of folate

First synthetized in 1945

More stable than natural form of folate

No active – Needs to be metabolized

Added in supplements and fortified foods

Tertiary Folate (3°) (6S)-5-MTHF   :

The concentration of 5-MTHF in cord serum is approximately 2 times higher than in maternal serum (mean 35.8 vs. 15.6 nmol/L), suggesting that 5-MTHF during pregnancy can provide an immediate source of folate to be transported to the fetus

(6S)-5-MTHF is the main folate form in cord blood (means 89.4% of total folate)

The folic acid that is found most commonly in vitamin supplements and fortified food is NOT folate.

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

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NAD Precursors: NAD Riboside and NMN/Resveratrol Powder Mix

NAD precursors : NAD Riboside and NMN/Resveratrol Powder Mix

Nicotinamide mononucleotide (NMN) is a nucleotide that is well known for its role as an intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis.

Two pathways are mainly followed in case of a eukaryotic human—one is through the salvage pathway using nicotinamide while the other follows phosphorylation of nicotinamide riboside.

Due to the unavailability of a suitable transporter, NMN enters inside the mammalian cell in the form of nicotinamide riboside followed by its subsequent conversion to NMN and NAD+.

This particular molecule has demonstrated several beneficial pharmacological activities in preclinical studies, which suggest its potential therapeutic use.
Mostly mediated by its involvement in NAD+ biosynthesis, the pharmacological activities of NMN include its role in :

  1. Cellular biochemical functions
  2. Cardioprotection
  3. Diabetes
  4. Alzheimer’s disease
  5. Complications associated with obesity.
  6. The recent groundbreaking discovery of anti-ageing activities of this chemical moiety has added a valuable essence in the research involving this molecule.

Nicotinamide mononucleotide (NMN) is a type of bioactive nucleotide which is naturally formed by the reaction between a phosphate group and a nucleoside containing ribose and nicotinamide.

In human cells, NMN is available as a source of cellular energy

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.

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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]
2. Pubchem Nicotinamide Mononucleotide|C11H15N2O8P—PubChem. [(accessed on 1 January 2019)]; Available online: https://pubchem.ncbi.nlm.nih.gov/compound/nicotinamide_mononucleotide.
3. Mills K.F., Yoshida S., Stein L.R., Grozio A., Kubota S., Sasaki Y., Redpath P., Migaud M.E., Apte R.S., Uchida K., et al. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016;24:795–806. doi: 10.1016/j.cmet.2016.09.013. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
4. Huang N., Sorci L., Zhang X., Brautigam C.A., Li X., Raffaelli N., Magni G., Grishin N.V., Osterman A.L., Zhang H. Bifunctional NMN Adenylyltransferase/ADP-Ribose Pyrophosphatase: Structure and Function in Bacterial NAD Metabolism. Structure. 2008;16:196–209. doi: 10.1016/j.str.2007.11.017. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
5. Berger F., Lau C., Dahlmann M., Ziegler M. Subcellular Compartmentation and Differential Catalytic Properties of the Three Human Nicotinamide Mononucleotide Adenylyltransferase Isoforms. J. Biol. Chem. 2005;280:36334–36341. doi: 10.1074/jbc.M508660200. [PubMed] [CrossRef] [Google Scholar]
6. Yoshino J., Mills K.F., Yoon M.J., Imai S. Nicotinamide mononucleotide, a key NAD(+) intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice. Cell Metab. 2011;14:528–536. doi: 10.1016/j.cmet.2011.08.014. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
7. Yamamoto T., Byun J., Zhai P., Ikeda Y., Oka S., Sadoshima J. Nicotinamide Mononucleotide, an Intermediate of NAD+ Synthesis, Protects the Heart from Ischemia and Reperfusion. PLoS ONE. 2014;9:e98972. doi: 10.1371/journal.pone.0098972. [PMC free article] [PubMed] [CrossRef] [Google Scholar]
8. Long A.N., Owens K., Schlappal A.E., Kristian T., Fishman P.S., Schuh R.A. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model. BMC Neurol. 2015;15:19. doi: 10.1186/s12883-015-0272-x. [PMC free article] [PubMed] [CrossRef] [Google Scholar]

Integrative Medicine Tools for Parkinson’s Disease Management

Some Integrative Medicine Tools for Parkinson’s Disease Management

As with other neurodegenarative diseases like multiple sclerosis and motor neuron disease, I would highly suggest low dose naltrexone 3-4.5mg at night. LDN elevates endorphins which orchestrate the activity of stem cells, natural killer cells and other immune cells.

LDN is thus effective for a multitude of disease states, see www.ldnscience.org

Transcranial light with LED infrared light is showing very promising results for Parkinsons and Alzheimer disease states alike.

Glutathione : L-dopa helps to temporarily reduce the symptoms of Parkinson’s disease, studies are now suggesting caution that L-dopa therapy may increase free radical production and ncrease oxidative stress, thus speeding up the progression of Parkinson’s disease. Low levels of glutathione are often present in parkinson’s patients. Glutathione helps to preserve brain tissue by preventing damage from free radicals. It also acts to recycle vitamins C and E which also reduce free radicals since theses are antioxidants. Glutathione is beneficial in Parkinson’s disease since it has the unique ability to make certain areas of the brain more sensitive to dopamine. Consequently, even though dopamine is decreased, it becomes more effective.

Detoxification : Parkinson’s patients have flaws in their ability to detoxify various chemicals to which they are exposed. Metal detoxification including pesticide, herbicide and aluminium and mercury detoxification are essential as part of the mangement. Acetaminophen / panado can reduce liver glutathione and should be avoided in Parkinson’s disease sufferers.

Emothion, Orally Absorbable Glutathione

Now Available 

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

“We know that infrared light can reduce Parkinson’s symptoms and offer protection to brain cells.”

Read about Transcranial Low Level Light Laser Therapy & LED Infrared Helmet Here

LED-blog

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.

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References

  1. Graham, D., et al., “Oxidative pathways for catecholamines in the genesis of neuromelanin and cytotoxic quinones,” Mol Pharmacol 1978; 14:633-43.
  2. Perry, T., et al., “Parkinson’s disease: a disorder due to nigral glutathione deficiency Neurosci Lett 1982; 33:305-
  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.
  4. Bains, J., et al., “Neurodegenerative disorders in humans:the role of glutathione in oxidative stressmediated neuronal death,” Brain Res Brain Res Rev 1997; 25(3):335-58.
  5. 5. Przedborski, S., et al., “Chronic levodopa administration alters mitochondrial respiratory chain ac
  6. Birkmayer, J., et al., “Nicotinamide adenine dinucleotide (NADH)—A new therapeutic approach to Parkinson’s disease: Comparison of oral and parenteral application,” Acta Neurol Scand 1993; 87 (146):32-35.
  7. Schults, C., et al., “Absorption, tolerability and effects on mitochondrial activity of oral coenzyme Q-10 in parkinsonian patients,” Neurology 1998; 50:793-795.
  8. Mortensen, S., et al., “Dose-related decrease of serum coenzyme Q-10 during treatment with HMG-CoA reductase inhibitors,” Mol Aspects of Med 1997; 18(Suppl.):S137-44.
  9. Golbe, L., et al., Case-control study of early life dietary factor in Parkinson’s disease,” Arch Neurol 1988; 45(12):1350-3.
  10. Fahn, S., et al., “The endogenous toxin theory of the etiology of Parkinson’s disease and a pilot trial of high-dose antioxidants in an attempt to slow the progression of the illness,” Ann NY Acad Sci 1989; 570:186-96.
  11. Steffen, V., et al., “Effect of intraventricular injection of 1-methyl-4-phenylpyridinium protection by acetyl-L-carnitine,” Huma Exp Toxicol 1995; 14:865-871.
  12. Olanow, C., et al., “Attempts to obtain neuroprotection in Parkinson’s disease,” Neurology 1997; 49(Suppl 1):S26-S33.
  13. Tanner, C., et al., “Liver abnormalities in Parkinson’s disease,” Geriatrics 1991; 46(1):60-63. Przedborski, S., et al., “Chronic levodopa administration alters cerebral mitochondrial respiratory chain activity,” Ann Neurol1993; 34(5):715-23.
  14. https://surfershealth.com.au/news/2020/05/01/parkinsons-disease-infrared-light-may-improve-the-guts-microbiome/?fbclid=IwAR0TyyC_EBvPiDB65cyxqr7TDfEF6cP6kpAv4x5PuJCNHR7-ZtVjS8F5n8o

Is There A Downside To Statin Use To Prevent Coronary Artery Disease And Is There A Bigger Picture To The Prevention Of Heart Disease?

Is There A Downside To Statin Use To Prevent Coronary Artery Disease And Is There A Bigger Picture To The Prevention Of Heart Disease?

Statin drugs work by inhibiting HMG-CoA-reductase in the liver which is required to synthesize cholesterol.     Infact “statin drugs inhibit not just the production of cholesterol, but a whole family of intermediary substances, many if not all of which have important biochemical functions in their own right” say Enig and Fallon (3)

Firstly statins deplete the body of coenzymeq10 (coq10), which is benefitial to heart and muscle function.    This depletion leads to fatigue, muscle weakness, soreness, and eventually heart failure.      Muscle pain and weakness, and rhabdomyolysis occurs when statins activate the atropine-1 gene, which plays a key role in muscle atrophy. (13)

This muscle pain and weakness may be an indication of tissue breakdown which can also cause kidney damage.

Statins have been linked to :

  1. an increased risk of polyneuropathy (nerve damage that causes pain in the hands and feet and trouble walking)
  2. dizziness
  3. cognitive impairment, including memory loss (14)
  4. is  a potential risk of cancer (15)
  5. decreased function of the immune system (16)
  6. depression (4)
  7. violent behaviour (6)
  8. liver problems, including a potential increase in liver enzymes (regular liver function monitoring is suggested)
  9. neurodegenerative disease like amyotrophic lateral sclerosis (17)
  10. impotence due to lowering of sex hormones
  11. lipoprotein (a)…a substance that is made of an LDL “bad cholesterol” part plus a protein (apoprotein a).   Elevated Lp(a) levels are a very strong risk factor for heart disease.    Statins do not lower Lp(a), infact they may increase it.

What are the numbers needed to treat (NNT)? (how many people have to take the drug to avoid one incident, such as a heart attack).     For example a NNT of 50 for heart attacks, equates to 50 people needing the drug to prevent 1 heart attack.

Business week did an excellent story and found the REAL numbers right on a pharmaceutical ad. (19)     At first glance the ad boasts that this particular statin reduces heart attacks by 36%.    There is an asterix though, and in smaller print the following appears : “That means in a large clinical study, 3% of patients taking a sugar pill or placebo had a heart attack compared to 2% using this particular statin”

What this means is that for every 100 people who took the drug for 3.3 years, 3 people on placebos, and 2 on the statin, had heart attacks.     This equates to 1 less person per hundred having a heart attack on this particular statin.

The 36% figure looks so much more impressive doesn’t it!

The answer is not merely to turn to a drug to lower your cholesterol and ldl as the so-called experts would have you believe.

It is inflammation and oxidative stress that causes ldl (“bad cholesterol”) to cause blood vessel disease (atherosclerosis).

Cholesterol has been described the last few decades as the smoking gun of heart disease.     Cholesterol per se is not the cause of heart disease.

You actually need cholesterol!

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 :

Cholesterol and Inflammation

Inflammation is sometimes a good thing as it is the body’s natural response to invaders it perceives as threats, in other words it helps the body heal. If your arteries are damaged however, a similar process occurs except the result is plaque formation.  This plaque , along with thickening of your blood and constriction of the blood vessels increases your risk for high blood pressure and heart attacks. Cholesterol comes into the picture, because it is necessary to replace the damaged cells. No cell can form without cholesterol. So the liver will generate more cholesterol when necessary to produce healthy cells.

The test normally performed to assess chronic inflammation is crp(c-reactive protein, preferably highly sensitive crp..<1, low risk, 1-2 moderate risk, >3 high risk for heart disease).

In the eyes of conventional medicine , when there is a raised cholesterol it is a sign of increased risk…is there a counter argument?

Sally Fallon, the president of the Weston A. Price foundation, and Mary Enig, PhD , an expert in lipid biochemistry, have gone so far as to call high cholesterol “an invented disease,a problem that emerged when health professionals learned how to measure cholesterol levels in the blood” (3)

What is the explanation? If you have increased levels of cholesterol, it as at least in part because of the increased inflammation in the body…this is to help the body heal and repair.

Conventional medicine recommend that lowering cholesterol is the way to reduce heart disease. Dealing with the inflammation and oxidative stress might be a better option!

As Dr Rosedale so rightly points out (2) “if excessive damage is occurring, such that is necessary to distribute extra cholesterol through the bloodstream, it would not seem wise to merely lower cholesterol and forget about why it is there in the first place.   It would seem much smarter to reduce the extra need for the cholesterol – the excessive damage that is occurring, the reason for the chronic inflammation.”

In 2006 a review in the Annals of Internal Medicine (8) found that there is insufficient evidence to support the target numbers outlined by the panel.    The authors of the review were unable to find research providing evidence that achieving a specific LDL target level was important in and of itself, and found that the studies attempting to do so suffered from major flaws.    Eight of the none doctors on the panel that developed the new cholesterol guidelines had been making money from the drug companies that manufacture statin cholesterol-lowering drugs (9).

According to data from Medco Health Solutions Inc., more than half of insured Americans are taking drugs for chronic health conditions.   And cholesterol lowering medications are the second most common variety among this group (high blood pressure medications—another vastly over-precribed category—were first) (11)

Disturbingly, as written in Business Week early in 2008, “Some researchers have even suggested—half jokingly –that the medications should be put in the water supply” (12)

Chronic inflammation is caused by, for example :

  1. oxidized cholesterol (cholesterol that has gone rancid, such as that from overcooked, scrambled eggs)
  2. eating lots of sugar and grains
  3. eating foods cooked at high temperatures
  4. eating trans fats
  5. a sedentary lifestyle
  6. smoking
  7. emotional stress

To lower cholesterol naturally :

  1. make sure that you are getting plenty of high-quality, animal based omega 3 fats like krill oil or heavy metal free omega 3 fishoil
  2. reduce grains and sugars
  3. eat the right foods fro your nutritional type
  4. eat a good proportion of raw foods
  5. eat healthy, preferably raw, fats that correspond to your nutritional type, including : olive oil, coconut and coconut oil, organic raw dairy products, avocados, raw nuts, seeds, eggs (lightly cooked with yolks intact or raw), organic grass fed meats.
  6. get the right amount of exercise
  7. avoid smoking and drinking excessively
  8. address your emotional challenges

Oxidation Theory

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 :

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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
25. Steinberg, D, et al, New England Journal of medicine 1989; 320:915-923
26. Cathcart, M.K.,et al Journal of of leukocyte biology 1985; 38:341-350
27. Tolonen, M, et al , Biologic and Trace Element research 1988; pp221-228
28. Salonen, J.T., et al, American Journal of Clinical nutrition 1991; 53(5) p1222-1229
29. Boorman, G.A.,et al , toxicol Pathol 1987; 15(4) p451-456
30. Petty, M.A. et al, European Journal of Pharmacology 1990; 180(1):119-127
31. Rath, M.,et al , Arteriosclerosis1989; 8:579-592
32. Rader, D.J., et al, Journal of the American Medial Association 1992; 267:1109-1111

“Zombie” Cells – Senolytics and Cellular Senescence

“Zombie” Cells – Senolytics and Cellular Senescence

Senescent cells are like “”Zombie”” Cells that no longer divide and release poisons to healthy cells

Cellular senescence is a state in which cells can no longer divide. … Therefore, the effects of cellular senescence in the organism vary according to a number of factors, such as age!      Very short telomeres can trigger senescence. However that’s only one of many causes :

  • DNA damage
  • Oncogenes
  • and stress can also make cells senescent

Cellular senescence has historically been viewed as an irreversible cell-cycle arrest mechanism that acts to protect against cancer, but recent discoveries in science has extended its knowledge in complex biological processes such as development, tissue repair, ageing and age-related disorders and now recommend removing senescent cells from the body

Senescent cell production occurs throughout life and plays beneficial roles in a variety of physiological and pathological processes including embryogenesis, wound healing, host immunity and tumor suppression.

Meanwhile, throughout life, the steady accumulation of senescent cells in the body with age also has an adverse negative consequence that leads to age related death. Senescent cells do not divide or support the tissues of which they are part; instead, they emit a range of potentially harmful chemical signals that encourage nearby cells to enter into the same senescent state.

Autophagy was originally thought to suppress cellular senescence by removing damaged macromolecules or organelles, yet recent studies also indicated that autophagy promotes cellular senescence by facilitating the synthesis of senescence-associated secretory proteins so a different strategy to remove the accumulation of senescent cells is needed.

A new class of drugs known as ‘Senolytics’ focuses on the destruction of these stubborn “death-resistant” senescent cells from the body in order to reduce inflammation and improve tissue function.

New research proposes removing senescent cells in order to promote healthy longevity.

Fisetin A Plant Flavonoid

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 An Everyday Maintenance Program

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

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Autophagy and mTOR – Inducing Supplements for Longevity

Autophagy and mTOR – Inducing Supplements for longevity

AUTOPHAGY AND AGING

One of the main catabolic processes of the body is called, ‘AUTOPHAGY’, which translates into self-devouring or self-eating. Autophagy is a metabolic process during which cells disassemble and remove their dysfunctional components. You’re basically recycling cellular debris and taking out the trash.

Autophagy has many longevity-boosting benefits:

1) Reduced inflammation
2) Stronger immune system
3) Suppressed cancer and tumor cells
4) Elimination of pathogens and toxins

Decreased cellular recycling and accumulation of molecular waste inside the cells are common to all aged cells. Diminishing autophagic pathways are said to play a major role in this type of aging.

Autophagy is good for longevity because you’ll be replacing old cellular material that’s causing you inflammation and oxidative stress with new and rejuvenated cells by converting the worn out cells into energy.

According to the mitochondrial theory of aging, reactive oxygen species damage mitochondria and decrease ATP production which leads to shorter life expectancy.       Therefore, autophagy is a critical component to preserving mitochondrial functioning and keeping your body youthful by eliminating the accumulation of free radicals.

AUTOPHAGY AND mTOR

Autophagy is regulated through the pathways of mTOR and AMPK.      They’re part of the Kinase Triad by promoting anabolism and catabolism respectfully.

mTOR inhibits the autophagy process because it supports cellular growth, whereas AMPK helps with autophagy because of nutrient deprivation.       When in an energy deficit, AMPK starts to block cellular growth by suppressing the mTORC1 pathway, which makes the body Catabolize its weakest parts to keep the healthy components in check.

Although autophagy is a catabolic process that involves protein breakdown, it’s needed for muscle homeostasis (balance)! It’s going to improve your body’s ability to cope with catabolic stressors such as exercise and fasting by helping to recycle energy and promote protein sparingness. However, dysfunctional autophagy contributes to aging through sarcopenia which is muscle loss!

At the same time, excessive autophagy can also lead to catabolism of lean tissue and muscle disorders, which again can accelerate premature aging and make you more prone to other metabolic diseases!

Your entire body and all cells are made of protein, which requires the presence of anabolic precursors and building blocks. That’s why you need mTOR and amino acids for existence and DNA repair.

THE DARK SIDE OF mTOR COMPLEX

(mTOR) Mammalian target of rapamycin promotes cellular growth, which is going to build new muscle tissue a state of anabolism! However, there’s a dark side to mTOR that’s not optimal for longevity!

(mTOR) is the master anabolic regulator that organizes many other nutrient sensors, such as insulin, leptin, and insulin-like-growth-factor (IGF-1).

IGF-1 is another hormone that supports growth development, healing, muscle building, and bone strengthening, depending on what the body needs. When the pituitary gland in your brain releases human growth hormone, then the liver will produce IGF-1 and stimulates anabolism!

Too high mTOR and IGF-1 levels are associated with different types of cancers.

Inhibiting IGF-1 has extended the lifespan of mice but there are no associations with humans.

Disrupted mTORC1 directly inhibits mitochondrial respiration, whereas decreased mTOR up regulates glycolysis and autophagy.

IGF-1 TO THE RESCUE

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.

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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!

Transcranial Low Level Light Laser Therapy and LED Infrared Helmet

Transcranial Low Level Light Laser Therapy & LED Infrared Helmet

The use of transcranial light has become increasingly popular in recent times for neurodegenerative diseases,  Alzheimers and parkinsons disease to name but a few.

It is also a therapy becoming increasingly popular for depression, stroke, and post traumatic brain injuries. Treatment time using the helmet to deliver transcranial light is typically  1-30 minutes.    Recommendation : 30 minutes/day is now possible with having your own LED helmet (retailing at 2900Euro)

Frequency from 1Hz to 20,000 Hz

The helmet is as individual as you are!

If cost is an issue, at least we can do the transcranial light lasert herapy at our clinic as frequently as required. Easy Handling LED Infrared Helmet comes with a US adapter with simple setup for Transcranial Low-Level Laser Therapy. Transcranial Low-Level Laser Therapy (TLLLT) is the direct irradiation of the human brain with highly focused infrared lasers.

Unlike other wavelengths, infrared light has the ability to penetrate bones and to bring light energy to the targeted brain areas. Light energy is absorbed by different types of cells to trigger a broad range of intra-cellular effects.

Transcranial Low Level Light Laser Therapy and LED Infrared Helmet Now Available At Dr Golding’s Medical Practice

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.

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Discover Underlying Medical Issues – Functional Lab Testing At Dr Golding’s

Discover Underlying Medical Issues – Functional Lab Testing At Dr Golding’s

So often, conventionally, routine lab testings are reported normal and the person/patient still knows that there are underlying medical issues….symptoms may be related to gut issues, fatigue, depression, anxiety, sleep disorders, mental health issues, sense of well-being, depleted energy, problems with weight and hormone imbalances and so on. With inetgrative and functional medicine we are more able to get to underlying causes of medical issues, and often functional lab testing is very useful in this regard.

Dr Craige Golding Medical practice now offers an array of functional lab tests to diagnose, with precision, the underlying causes that one needs to address for optimum health and longevity.

There is a new standard of care emerging in medicine, and recent science in molecular medicine has challenged the fatalistic approach to the mere management of disease with the pharmaco-therapeutic approach.

The predisposition model recognizes that we all inherit genetic vulnerability, but it incorporates unfolding evidence that environmental and nutritional factors interact with our genome to produce a unique phenotype and the eventual clinical outcome. In order to identify the causative determinants that must be addressed in clinical situations, an objective mechanism is required to explore those nutritional and toxicological factors that are contributing on a molecular basis to health outcomes. Accordingly, laboratory testing to evaluate biochemical, toxicological and nutritional status in individual patients is an absolute prerequisite in modern health care to adequately investigate and manage health problems, particularly in patients with complex problems

Some of the functional lab tests available at the practice include (current prices included) :

  • Urine Organic Acids (U-OAT) : R2 795.00
  • Urine Amino Acids (U-AAT) : R2 795.00
  • Combo U-OAT & U-AAT : R4 895.00
  • Dried Bloodspot (DBS) Amino Acid Test : R1 895.00
  • Combo U-OAT & DBS Amino Acids Test : R4 195.00
  • GI-MAP™ (DNA qPCR stool analysis) : R7 145.00
  • GI-MAP™ + Zonulin : R7 945.00
  • Hair Tissue Mineral Analysis Test : R3 145.00
  • Oligoscan : R 850
  • Helicobacter pylori : R395
  • Nutrismart (food allergy/sensitivity testsing) : R 2500
  • Urine dipstix : R27
  • Salva ph : R 20
  • Saliva hormone testing : R600 approximately per hormone.
  • VIOME: R 3290 for test plus R 700 for test kit.
  • Extensive nutrigenomic and genetic testing : R4400
  • Bone density (cuba sonar) : R 365
  • DUTCH TEST (urine steroid metabolites) : cost (GBP 345)
  • TELOYEARS (telomere testing) : cost R3845
  • MYCOTOXIN urine testing (toxic mould exposure screening) : cost R9265
  • Heavy metal screening urine : post DMSA challenge/provocation : DMSA costs R90 for 600mg and R120 for 800mg, plus lab urine urine heavy metal cost
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Let Food Be Your Medicine – Viome Testing Now At Dr Goldings

Let Food Be Your Medicine!

Do any of the following issues hold true for you or a loved one? Have you considered these solutions?

Issue: Despite my dieting, I can’t maintain my weight.
Solution: No one diet is right for everyone.

Issue: I can’t focus during the day.
Solution: Your brain uses more energy than any other tissue in your body. In order for your brain to work, you need to eat a combination of foods that will optimize your body’s energy production and enhance your focus.

Issue: I feel bloated after almost every meal.
Solution: If you aren’t eating the right foods for your microbiome, you can feel the consequences. Viome identifies the ideal diet to help your gut thrive.

Issue: I don’t have the energy to do the things I love.
Solution: The food you eat gets processed into energy. When you eat the foods that are right for your microbiome and biochemistry, this process becomes efficient—resulting in maximal energy.

Issue: I have trouble falling asleep and staying asleep.
Solution: Your microbiome affects your biological clock. An analysis of your microbiome will provide the needed information to help you maintain it at its most healthy functioning level, which may improve your sleep.

For many people, the issues are widespread, and may feel inescapable. While so many of us and our loved ones, colleagues, and acquaintances struggle with these issues, for most, the given solutions are unfamiliar. The solutions use words such as “microbiome” and suggest connections that we haven’t encountered before. From reading these solutions, you might be left wondering:

What’s a “microbiome”?

What’s the relationship between my “microbiome” and my health?

How can I harness my “microbiome” to optimize my health and well-being?

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Find Out How to Harness Your Microbiome

Book Your Appointment Today
011 718 3004 / 011 483 1080

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.

Book your appointment and find what your unique gut michrobiome requirements are and how to optimize your health and well-being.

Phosphocomplex® Liver Protection – Now Available At Dr Golding’s Medical Practice

Phosphocomplex® Liver Protection – Now Available At Dr Golding’s Medical Practice

Phosphocomplex® is the proprietary bioavailable Sylibin, in the form of a lipid-compatible active compound where the Silybin has been complexed with phospholipids. Silybin is the most abundant and potent constituent of silymarin, the most active ingredient of milk thistle plant (Silybum marianum) that has been extensively studied for its benefits in liver health. Through its antioxidant and anti-inflammatory effects, the Silybin contained in Phosphocomplex® has the capacity to protect and normalize liver functions, also promoting the production of glutathione.

Unfortunately, Silybin has a poor intestinal absorption and a low bioavailability. In Phosphocomplex®, the phospholipid complexation of Silybin occurs with phosphatidylcholine, which is an important emulsifier in the gastrointestinal tract and improves the capacity of the Silybin to cross the lipid-rich bio-membranes and reach circulation, resulting in enhanced bioavailability. The enhanced bioavailability of Phosphocomplex® has been tested in comparison with a formulation purchased from the nutraceutical market and used as reference product. Silybin (from Silybum, the generic name of the plant from which it is extracted), is the major active constituent of silymarin, a standardized extract of the milk thistle seeds, containing a mixture of flavonolignans consisting of silibinin, isosilibinin, silicristin, silidianin and others. Silybin itself is a mixture of two diastereomers, silybin A and silybin B, in approximately equimolar ratio.

Silybin has been used for centuries to address liver health, due to the recognized role in liver protection and detoxification. There are clinical evidences for the use of silybin as a supportive element in alcoholic and non alcoholic steatohepatitis (Fatty liver disease) and chronic liver disease (Cacciapuoti et al., World Journal of Hepatology, 5 (3), 109–113, 2013).
Silybin has an important role in liver protection and detoxification. It inhibits lipid peroxidation, it supports a good cell functionality and neutralizes the excess of free radicals thus reducing the oxidative stress in the liver. The effective antioxidant property of Silybin allows to conserve Glutathione (GSH) in liver cells while stabilizing the liver cells membranes against oxidative attack.

Several studies have also demonstrated that Silybin stimulates synthesis and activity of enzymes responsible for detoxification pathways in liver and also blocks the oxidative toxicities of alcohol, carbon tetrachloride and mushroom toxins. Silybin is poorly absorbed by the intestine, that limits its benefits because of :

  • Multiple-ring large size molecules which cannot be absorbed by simple diffusion
  • Poor miscibility with lipids, severely limiting their ability to pass across the lipid-rich outer membranes of the enterocytes of the small intestine
  • Extensive phase II metabolism and rapid excretion in bile and urine, The poor water solubility and bioavailability of silybin have inspired to the development of enhanced formulations to increase its absorption. A complex of silybin and phospholipids has shown to be about 10 times more bioavailable than silybin itself (Kidd P. et al., Alternative Medicine Review: a Journal of Clinical Therapeutic 10 (3): 193–203,2005.

Biological & Functional Roles In A Healthy Liver

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

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