Tag Archives: CoQ10

Eat your greens – chlorophyll metabolites in our blood may be maintaining our blood anti-oxidants.

  • Eat your greens!
    Eat your greens!

    Everyone knows about CoQ10, with many people frequently taking it for ‘vascular health’ . It is true that ubiquinol in the blood stream is an anti-oxidant that helps maintain vascular integrity. Ubiquinol–10  is an endogenously synthesized lipid antioxidant that scavenges free radicals and is involved in a-tocopherol homeostasis. It prevents lipid peroxidation and in the process is oxidized to ubiquinone.

  • 95 % of the quinone is maintained as ubiquinol, which must be regenerated from ubiquinone after it prevents lipid oxidation.
  • The study below demonstrated derivatives of chlorophyll can catalyze the reduction of ubiquinone to generate ubiquinol in plasma. The chlorophyll in our system is obtained from green leafy vegetables, and it is derivatives of the chlorophyll that may be catalyzing the reforming of ubiquinol, rather than ascorbic acid, carotenoid, tocopherol and flavonoid antioxidants that are usually given the credit for this process.
  • In the blood stream, metabolites of chlorophyll , such as chlorophyllide a, pheophytin-a, pheophorbide-a, methyl pheophorbide-a, 10-OH-pheophorbide-a, 10- OH-methyl pheophorbide-a, pyro pheophorbide-a and methyl pyropheophorbide are formed and may catalyze the photoreduction of ubiquinone to ubiquinol.
  •  Both light and light-absorbing chlorophyll metabolites can be present in capillaries, arteries and veins of several animals including humans. If chlorophyll metabolites catalyze the photoreduction of plasma ubiquinol in vivo, it would be a novel mechanism to maintain high levels of plasma ubiquinol – and this is what the paper listed in it’s research proposes, is that light through our skin drives chlorophyl metabolites to regenerate the phytonutrient ubiquinol.
  • Dietary Chlorophyll Metabolites Catalyze the Photoreduction of Plasma ubiquinone
  • Bottom line: Eat your greens and get sunshine!

Consumption of fruits and vegetables was inversely associated with stroke incidence, stroke mortality, ischemic heart disease mortality, and CVD mortality.

Known modifiable risk factors for CVD include smoking, sedentary lifestyle, diet, dyslipidemia, hypertension, obesity, and type 2 diabetes.

The observed protective effect of consuming plant foods on chronic diseases is likely due to their bioactive components.

Plant Bioactives:

  1. Phytosterols are naturally-occurring plant sterols found in the non-saponifiable fraction of plant oils. Plants synthesize several types of phytosterols (e.g., sterols and stanols) that are structurally similar to cholesterol, except for the functional group substitutions on the sterol side chain at the C24 position. Beta-sitosterol (most abundant), campesterol, and stigmasterol comprise almost our entire intake of phytosterols. Since humans do not synthesize phytosterols, they must be obtained from the diet. The main dietary sources of naturally-occurring phytosterols are vegetable oils, nuts, grains and, to a lesser extent, fruits and vegetables. Commonly consumed products that are fortified with phytosterols, such as Benecol™ and Take Control™ are found in many foods. . Benecol spread contains stanol esters derived from tall oil (pine tree wood pulp) and Take Control margarine contains sterol esters from soybeans. Consuming 2–3 g/d of phytosterols from these products resulted in approximately 14% reduction in LDL  with no change in HDL. Thus, both sterols and stanols are equally effective in lowering LDL concentration. NCEP ATP 111 guuidelines: two grams of plant sterol or stanol esters daily for optimal dietary therapy for elevated LDL.
  2. Flavonoids: The most common flavonoids are flavones, flavanols, catechins, and anthocyanins, along with anthoxanthins. There is an inverse relationship between flavonoid intake and chronic diseases including CVD. Red wines contain an abundance of polyphenols including phenolic acids (for example, gallic acid, and caffeic acid), stilbenes (resveratrol), and flavonoids (for example, catechin, epicatechin, quercetin, rutin) . Gallic acid has more antioxidant activity than caffeic acid. Wine polyphenols can induce vasorelaxation via nitric oxide synthesis , decrease platlet aggregation, and decrease inflammatory mediators. Resveratrol is a polyphenol found principally in the skin of grapes and, in lesser amounts, in peanuts. It inhibits both LDL oxidation and platelet aggregation and scavanges free radicals.
  3. Lignans: Lignans are polyphenols found in plants, especially in flaxseed (secoisolariciresinol diglucoside), sesame seeds (sesamin, sesamolin), and soy, followed by whole-grains cereals (syringaresinol), and legumes, including nuts. Fruits and vegetables contain a wide variety of lignans (e.g., matairesinol (MAT), pinoresinol (PINO) and lariciresinol (LARI)) but in minute quantities. The proposed mechanisms by which dietary lignans could reduce the risk of CVD include the phytoestrogenic, and antioxidant activity of these compounds and their metabolites. Some plant lignans such as matairesinol (MAT), secoisolariciresinol (SECO), pinoresinol (PINO), and lariciresinol (LARI) are metabolized by intestinal bacteria to enterolignans (enterodiol and enterolactone) in various proportions.
  4. Resistant starches: Complex carbohydrates derived from starch contribute over half of humans’ daily energy requirements. Starch is a homopolysaccharide made in plants and stored in granules. Amylose and amylopectin are two polymers found in starch and are identified based on the glycosidic bond linking the α-D-glucose monomers. Amylose is a linear polymer with α-(1,4) linkages while amylopectin has linear α-(1,4) linkages and α-(1,6) branch points. There are four types of resistant starches – types one to four. Dietary sources of RS 1 include partially milled grains and seeds. RS 2 can be found in raw potatoes, legumes, just-ripe bananas, and high-amylose maize (HAM). RS 3 results from retrograded foods, such as potatoes, cereals, and breads. Chemically- or physically-modified starch and resistant maltodextrins are known as RS 4 and 5, respectively.  Due to lack of enzymatic hydrolysis, the direct contribution of glucose to blood from RS is minimal and allows for an attenuated post-prandial glycemic response.  Peripheral insulin sensitivity (Si) also improved by approximately 20% in individuals with metabolic syndrome consuming the same amount or RS.  There is  production of short chain fatty acids (SCFA) from RS fermentation by gut microbiota in the large intestine which tereby makes RS bioactive. The SCFA are capable of influencing risk, and even treatment, of NCDs such as diabetes and cancer through several mechanisms: decreasing luminal pH, enhancing mineral absorption, and stimulating the release of two satiety peptides known as glucagon-like peptide -1 (GLP-1) and peptide tyrosine tyrosine (PYY) to the periphery . RS can act as a prebiotic to selectively increase the concentration and viability of certain bacteria, such as Ruminococcus bromii .Intra-individual variation in gut microbiota may influence RS fermentation, the production of SCFA, and upregulation of GLP-1.
  5. Cyclic Dipeptides: Cyclic dipeptides (also known as 2,5dioxopiperazines; 2,5-diketopiperazines; cyclo (dipeptides); or dipeptide anhydrides) are relatively simple compounds and, therefore, are among the most common peptide derivatives found in nature. Consistent with a role for fermentation process in synthesis of cyclic dipeptides is the observation of high levels of cyclo (His-Pro) in foods that undergo fermentation and/or high heat treatment of protein-rich foods. Such examples are nutritional supplements (e.g., TwoCal HN and Jevity), milk, yogurt, sauces, and fermented fish . Active cyclic dipeptides include cyclo (His-Pro), cyclo (Leu-Gly), cyclo (Tyr-Arg), and cyclo (Asp-Pro). Of these only cyclo (his-Pro)[CHP] has been shown to be endogenous to animal kingdom. CHP may act as an appetite suppressant and satiety-inducer.  There is a possible role of CHP in insulin secretion and glucose metabolism.  CHP  causes higher insulin excursions without any change in C-peptide suggesting that CHP may decrease hepatic insulin clearance.    Items with CHP include tuna, fish sauce, Dried Shrimp , Spent Brewer’s Yeast hydrolysate, and others.
  6. Fruit Berries:  Polyphenols found in berries and other plant foods are particularly associated with anti-inflammatory, antioxidant, cardioprotective, and chemopreventive properties. Several compounds contribute to the antioxidant properties of berries and are typically found in the outer parts of the fruit or berry, most often as cinnamic and/or benzoic acid derivatives. Tanins, Anthocyanins,  carotenoids and stilbenes such as resveratrol are present in berries. Some amounts of resveratrol can be found in cranberries, strawberries, and other berries. Chokeberry, bilberry, and blackcurrant berries have the highest antioxidant capacity of the different berry fruits (umol Trolox/g fresh weight), and whole fruit extracts have greater antioxidant activity than many isolated phenolic compounds or vitamins . Strawberries are known to be high in phenolic compounds such as the phenolic acid derivative ellagic acid, and contain a significant amount of vitamin C. Blueberries are noted for a wide variety of anthocyanin compounds, while both cranberries and blueberries also contain significant concentrations of phenolic acids. Anti-oxidants in  Berries provide  anti-inflammatory activity, free radical scavenging and up-regulation of antioxidant enzyme genes, decreased levels and antioxidation of LDL, increases in circulating HDL, inhibition of platelet activation and aggregation, and improvements in endothelial function. Berries have been shown to provide improvements in blood pressure or hypertensive status due to increased NO bioavailability via activation of endothelial NO synthase.

Bioactive Plant Metabolites in the Management of Non-Communicable Metabolic Diseases

Statins’ effect on plasma levels of Coenzyme Q10 and improvement in myopathy with supplementatio

Light-harvesting chlorophyll pigments enable mammalian mitochondria to capture photonic energy and produce ATP  <– we show that mammalian mitochondria can also capture light and synthesize ATP when mixed with a light-capturing metabolite of chlorophyll. To demonstrate that dietary chlorophyll metabolites can modulate ATP levels, we examined the effects of the chlorophyll metabolite pyropheophorbide-a (P-a) on ATP synthesis in isolated mouse liver mitochondria in the presence of red light (lmax5670 nm), which chlorin-type molecules such as P-a strongly absorb (Aronoff, 1950), and to which biological tissues are relatively transparent. We used P-a because it is an early metabolite of chlorophyll, however, most known metabolites of chlorophyll can be synthesized from P-a by reactions that normally take place in animal cells The same metabolite fed to the worm Caenorhabditis elegans leads to increase in ATP synthesis upon light exposure, along with an increase in life span.   Results suggest chlorophyll type molecules modulate mitochondrial ATP by catalyzing the reduction of coenzyme Q, a slow step in mitochondrial ATP synthesis. We propose that through consumption of plant chlorophyll pigments, animals, too, are able to derive energy directly from sunlight. We show that dietary metabolites of chlorophyll can enter the circulation, are present in tissues, and can be enriched in the mitochondria. When incubated with a light-capturing metabolite of chlorophyll, isolated mammalian mitochondria and animal-derived tissues, have higher concentrations of ATP when exposed to light, compared with animal tissues not mixed with the metabolite. The hypothesis is that photonic energy capture through dietary-derived metabolites may be an important means of energy regulation in animals.

  • To synthesize ATP, mitochondrial NADH reductase (complex I) and succinate reductase (complex II) extract electrons from NADH and succinate, respectively. These electrons are used to reduce mitochondrial CoQ10, resulting in ubiquinol (the reduced form of CoQ10). Ubiquinol shuttles the electrons to cytochrome c reductase (complex III), which uses the electrons to reduce cytochrome c, which shuttles the electrons to cytochrome c oxidase (complex IV), which ultimately donates the electrons to molecular oxygen. As a result of this electron flow, protons are pumped from the mitochondrial matrix into the inner membrane space, generating a trans-membrane potential used to drive the enzyme ATP-synthase.
  • Photons of red light from sunlight have been present deep inside almost every tissue in the body. Photosensitized electron transfer from excited chlorophyll-type molecules is widely hypothesized to be a primitive form of light-to-energy conversion that evolved into photosynthesis. Electrons would be transferred by a metabolite of chlorophyll to CoQ10, from a chemical oxidant present in the mitochondrial milieu. Many molecules, such as dienols, sulfhydryl compounds, ferrous compounds, NADH, NADPH and ascorbic acid, could all potentially act as electron donors. Intense red light between 600 and 700 nm has been reported to modulate biological processes. . Exposure to red light is thought to stimulate cellular energy metabolism and/or energy production by, as yet, poorly defined mechanisms. On a clear day the amount of light illuminating your brain would allow you to comfortably read a printed book. Photons between 630 and 800 nm can penetrate 25 cm through tissue and muscle of the calf . Adipose tissue is bathed in wavelengths of light that would excite chlorophyll metabolites. Utilization of these facts may have the potential for new therapies. A potential pathway for photonic energy capture is absorption by dietary-derived plant pigments. Dietary metabolites of chlorophyll can be distributed throughout the body where photon absorption may lead to an increase in ATP .

Chlorophyll-related compounds inhibit cell adhesion and inflammation in human aortic cells.

Chlorophyll Revisited Anti-inflammatory Activities of Chlorophyll a and inhibition of expression of TNFa

An Evidence Based Systematic Review of Chlorophyll by the Natural Standard Research Collaboration

An Evidence Based Systematic Review of Goji Lycium spp by the Natural Standard Research Collaboration

Risk of new-onset diabetes associated with statin use




Insane Medicine – Inflammation and it’s risks.

Inflammation in the body breaks it down over time. Inflammation results from and, in part, causes autoimmune disorders and atherosclerosis with subsequent coronary artery disease and stroke. There are many ways to measure levels of inflammation in the body, but none are sensitive or specific for any particular condition. Likewise, inflammatory markers don’t always point to a specific treatment, but rather the presence of a system that is in trouble and needs thorough evaluation.

  • Inflammatory risk can be determined, in part, by elevations in C-reactive protein (CRP) and fibrinogen, which are both made in the liver as a result of the influence of cytokines such as interleukin-Ib, Interleukin-6 (IL-6), and Tumor necrosis Factor- alpha (TNF). Fibrinogen increases can increase your risk of platelet aggregation (clots) which increase stroke and heart attack risk.
  • There is evidence that DHEA and fish oil can decrease cytokine levels and decrease inflammation. Vitamin K can suppress IL-6 especially and thus decrease inflammatory markers. Nettle leaf extract has been found to suppress TNF-alpha and IL-1b cytokines. Aspirin, green tea, ginko bilboa, garlic, and Vitamin E have been found to decrease platelet aggregation and help blood flow, helping to avoid strokes and heart attacks. Lower fibrinogen levels may decrease the risk of myocardial infarction. Increased vitamin A levels decrease fibrinogen levels. Olive oil and fish have had a similar effect. Niacin (1000 mg a day) and vitamin C (2000 mg a day) will decrease fibrinogen. Bromelain (2000 mg/day) and EPA/DHA from fish oil also have a beneficial impact as well.
  • Elevated homocysteine levels also represent a cardiovascular threat. Elevated homocysteine prevents fibrinogen breakdown by inhibiting tissue plasminogen activator. Ways to diminish homocysteine levels and it’s risk include vitamin B12, vitamin B6, and trimethylglycine (TMG).
  • So elevations of homocysteine will increase your heart attack and stroke risk. Trimethylglycing (TMG) methylates homocysteine and converts it to methionine and s-adenosylmethionine (SAMe). In this process, the body needs folate and vitamin B-12. Homocysteine can also be removed from the body by the transsulfuration pathway using a vitamin B-6 dependent cystathione synthase enzyme. Vitamin B6 is necessary for this, and in some individuals, they lack the ability to produce the active form of vitamin B-6 (pyridoxal-5-phosphate), in which case, pyridoxal-5-phosphate can be supplemented instead to lower homocysteine.
  • So vitamins and supplements that decrease homocysteine to help preserve cardiovascular health include: TMG (500 mg a day), folate (800 mcg a day), vitamin B12 (200 mcg a day), inositol (250 mg a day), zinc (30 mg a day), and vitamin B6 (100 mg a day).
  • C-reactive protein: an inflammatory risk marker that increases under the influence of cytokines IL-6, IL-1B, and TNF-alpha. When elevated, heart attack risk increases by over two-fold .Studies have found that the statin rosuvastatin (Crestor) can decrease CRP levels and the inflammatory risk of heart attacks. Also helpful are aspirin, vitamin E, nettle leaf extract, DHEA, and fish oil.

So here is a basic list of inflammatory markers and cardiovascular risk markers that should be followed:

  1. Fibrinogen
  2. CRP
  3. Homocysteine
  4. Iron
  5. Glucose
  6. Cholesterol (HDL and LDL and triglycerides)
  7. DHEA
  • Obesity is a risk marker for heart attacks and cancer. Why is this? Increased circulating insulin and insulin resistance causes increased fat conversion of glucose and increased fat deposition. The increased insulin causes certain cancer types to grow as well as it serves as a growth factor.
  • The keys to successful strategies for health besides weight loss, include:
  1. Blood pressure control
  2. Glucose control
  3. Decreased LDL cholesterol
  4. Increasing your healthy HDL cholesterol
  5. Decreasing inflammatory markers such as fibrinogen, CRP, homocysteine, and cytokines.

Exercise is important. Be certain to consult your doctor before starting any exercise regimen. Use and exercise every muscle, every day. Exercise increases blood flow and lymph drainage increases. It also builds strength and flexibility, as well as balance and decreased falling risk. You feel less depressed and have more energy.

  • Coenzyme Q10: (Ubiquinone) is beneficial for heart and brain functioning, as well as being a blood pressure lowering supplement. Cells need it for energy production in the mitochondria and deficiency is found in aging and a variety of degenerative disorders. Muscles and the brain have high numbers of mitochondria which need this supplement. Taken orally, CoQ10 is absorbed and incorporated into the mitochondria. As one ages, the body produces only half of what it should of this vital supplement. Dosing is 30-300 mg a day. Of note, statins (anti-cholesterol agent) destroy co Q 10, so it is very helpful to take co Q10 supplements while on any statin. There are studies demonstrating increased energy production in the brain and muscles with Co Q10 supplementation, and it has been noted that there is an antioxidant protective ability as well provided by coQ10. In fact, there is speculation that Parkinson’s disease may result, in part, by reductions of co Q 10 levels in the brain (35% less than normal controls) and that with supplementation, some patients with Parkinson’s disease have had diminished progression of the disorder. As we age, Parkinson’s disease becomes more common, and it may be due to mitochondrial dysfunction and oxygen free radical production due to co-Q10 deficiency which results in the loss of neurons, thereby producing Parkinson’s disease. There is suggestion that dosages of coQ10 up to 1200 mg a day (which has minimal side-effects) seems to diminish the progression of Parkinson’s disease in some patients. This may be a result of the preservation of mitochondrial function.

…more to be added soon!