How to make your own CoQ10

Image Credit: Robert Owen-Wahl / Pixabay. This image has been modified

Chlorophyll is the green pigment that makes green leaves green. If you search for chlorophyll in the medical literature, a lot of what you find is about fecal fluorescence, a way to detect the contamination of carcasses in the slaughterhouse with feces to reduce the risk of food poisoning from pathogens harbored within animal feces. Fecal matter gets on meat either “with knife entry through the hide into the carcass, and also splash back and aerosol [airborne] deposition of fecal matter during hide removal”—that is, when they’re peeling off the skin. If, however, the animals have been eating grass, you can pick up the poo with a black light. As you can see in my video How to Regenerate Coenzyme Q10 (CoQ10) Naturally, a solution of chlorophyll is green, but, under a UV light, it lights up as red. So, if you have a black light in a chicken slaughter plant, you can get a drop on the droppings. The problem is most chickens aren’t outside anymore. They’re no longer pecking at grass so there’s less fecal fluorescence. We could let them run around outside or we could save money by just adding a chlorophyll supplement to their feed so we can better “identify areas of gut-spill contamination” on the meat.

The reason I was looking up chlorophyll was to follow-up on the data I presented in my Eating Green to Prevent Cancer video, which suggests that chlorophyll may be able to block carcinogens. I found a few in vitro studies on the potential anti-inflammatory effects of chlorophyll. After all, green leaves have long been used to treat inflammation, so anti-inflammatory properties of chlorophyll and their break-down products after digestion were put to the test. And, indeed, they may represent “valuable and abundantly available anti-inflammatory agents.” Maybe that’s one reason why cruciferous vegetables, like kale and collard greens, are associated with decreased markers of inflammation.

In a petri dish, for example, if you lay down a layer of arterial lining cells, more inflammatory immune cells stick to them after you stimulate them with a toxic substance. We can bring down that inflammation with the anti-inflammatory drug aspirin or, even more so, by just dripping on some chlorophyll. Perhaps that’s one of the reasons kale consumers appear to live longer lives.

As interesting as I found that study to be, this next study blew my mind. The most abundant energy source on this planet is sunlight. However, only plants are able to use it directly—or so we thought. After eating plants, animals have chlorophyll in them, too, so might we also be able to derive energy directly from sunlight? Well, first of all, light can’t get through our skin, right? Wrong. This was demonstrated by century-old science—and every kid who’s ever shined a flashlight through her or his fingers, showing that the red wavelengths do get through. In fact, if you step outside on a sunny day, there’s enough light penetrating your skull and going through to your brain that you could read a book in there. Okay, so our internal organs are bathed in sunlight, and when we eat green leafy vegetables, the absorbed chlorophyll in our body does actually appear to produce cellular energy. But, unless we eat so many greens we turn green ourselves, the energy produced is probably negligible.

However, light-activated chlorophyll inside our body may help regenerate Coenzyme Q10. CoQ10 is an antioxidant our body basically makes from scratch using the same enzyme we use to make cholesterol—that is, the same enzyme that’s blocked by cholesterol-lowering statin drugs. So, if CoQ10 production gets caught in the crossfire, then maybe that explains why statins increase our risk of diabetes—namely, by accidently also reducing CoQ10 levels in a friendly-fire type of event. Maybe that’s why statins can lead to muscle breakdown. Given that, should statin users take CoQ10 supplements? No, they should sufficiently improve their diets to stop taking drugs that muck with their biochemistry! By doing so—by eating more plant-based chlorophyll-rich diets—you may best maintain your levels of active CoQ10, also known as ubiquinol. “However, when ubiquinol is used as an antioxidant, it is oxidized to ubiquinone. To act as an effective antioxidant, the body must regenerate ubiquinol from ubiquinone,” perhaps by using dietary chlorophyll metabolites and light.

Researchers exposed some ubiquinone and chlorophyll metabolites to the kind of light that makes it into our bloodstream. Poof! CoQ10 was reborn. But, without the chlorophyll or the light, nothing happened. By going outside we get light and, if we’re eating our veggies, chlorophyll, so maybe that’s how we maintain such high levels of CoQ10 in our bloodstream. Perhaps this explains why dark green leafy vegetables are so good for us. We know sun exposure can be good for us and that eating greens can be good for us. “These benefits are commonly attributed to an increase in vitamin D from sunlight exposure and consumption of antioxidants from green vegetables”—but is it possible that these explanations might be incomplete?

Advantages of Soy

Tofu, soymilk, miso, tempeh, edamame—these and other soy products, including the soybeans themselves, are high in nutrients you tend to associate with other legumes, including fiber, iron, magnesium, potassium, protein, and zinc.

Soybeans naturally contain a class of phytoestrogens called isoflavones. People hear the word “estrogen” in the word “phytoestrogens” and assume that means soy has estrogen-like effects. Not necessarily. Estrogen has positive effects in some tissues and potentially negative effects in others. For example, high levels of estrogen can be good for the bones but can increase the likelihood of developing breast cancer. Ideally, you’d like what’s called a “selective estrogen receptor modulator” in your body that would have proestrogenic effects in some tissues and antiestrogenic effects in others. Well, that’s what soy phytoestrogens appear to be. Soy seems to lower breast cancer risk, an antiestrogenic effect, but can also help reduce menopausal hot-flash symptoms, a proestrogenic effect. So, by eating soy, you may be able to enjoy the best of both worlds.

What about soy for women with breast cancer? Overall, researchers have found that women diagnosed with breast cancer who ate the most soy lived significantly longer and had a significantly lower risk of breast cancer recurrence than those who ate less. The quantity of phytoestrogens found in just a single cup of soymilk may reduce the risk of breast cancer returning by 25 percent. The improvement in survival for those eating more soy foods was found both in women whose tumors were responsive to estrogen (estrogen-receptor positive breast cancer) and those whose tumors were not (estrogen-receptor negative breast cancer). This also held true for both young women and older women. In one study, for example, 90 percent of the breast cancer patients who ate the most soy phytoestrogens after diagnosis were still alive five years later, while half of those who ate little to no soy were dead.

Soy consumption has also been shown to benefit our kidneys, which appear to handle plant protein very differently from animal protein. Within hours of eating meat, our kidneys rev up into hyperfiltration mode. But, an equivalent amount of plant protein causes virtually no noticeable stress on the kidneys. Eat some tuna, and within three hours, your kidney filtration rate can shoot up 36 percent. But eating the same amount of protein in the form of tofu doesn’t appear to place any additional strain on the kidneys.


Bad Fat May Hurt Brain Function Over Time…

... But researchers report that ‘good’ fat may help preserve thinking and memoryobesity

This study supports others that have found an association between saturated fats, the incidence of Alzheimer’s disease and an increased decline in brain function, Samantha Heller, a dietitian, nutritionist, exercise physiologist and clinical nutrition coordinator at the Center for Cancer Care at Griffin Hospital in Derby, said.

“… it appears that the effects of eating a lot of saturated fat and the foods associated with it, such as red and processed meats, cheese and butter, over time creates a cascade effect of ill health.” Read the whole article

Source: / Picture Credit: Wikimedia Commons

Vegetarian Diet, Seventh Day Adventists and Risk of Cardiovascular Mortality

Vegetarian diet, Seventh Day Adventists and risk of cardiovascular mortality: A systematic review and meta-analysis.

Aus der MMW Fortschritte der Medizin 13. Nov. 2014 / Sonderheft 2 Seite 7

“Studien, die sich mit vegetarischer Ernährung befassen, nehmen oft Personen in den Blick, die aus weltanschaulichen Gründen auf tierische Nahrungsmittel verzichten, wie etwa die Siebenten-Tags-Adventisten.
Forscher der Universität Manchester (1) haben in einer Metaanalyse von acht Studien zum Vegetarismus mit insgesamt mehr als 180.000 Probanden gezeigt, dass sich die religiöse Ausrichtung durchaus auf die Resultate auswirken könnte. So führte vegetarische Nahrung hinsichtlich der Gesamtmortalität in allen drei Studien, die Adventisten einbezogen, zu Risikoreduktionen zwischen 20% und 50% im Vergleich zu Nichtvegetariern. Waren hingegen keine Adventisten vertreten – wie etwa in der EPIC-Oxford-Studie von 2013 oder der Vegetarierstudie des Deutschen Krebsforschungszentrums von 2005 -, ließen sich keine positiven Effekte der vegetarischen Diät nachweisen. Gleiches galt bezüglich zerebrovaskulären Erkrankungen.
Die Autoren erklären dies damit, dass der Adventismus nicht nur aus Essensvorschriften bestehe. Adventisten rauchen auch seltener und leben insgesamt gesünder. Sie werden zum Alkohol- und Drogenverzicht, zu regelmäßiger körperlicher Betätigung, genügend Schlaf und stabilen psychosozialen Beziehungen ermuntert.
“Zusammengefasst geht die Verminderung von KHK und Gesamtsterblichkeit unter vegetarischer Ernährung hauptsächlich auf die Adventistenstudien zurück”, so die Autoren. Studien in anderen Populationen hätten weniger überzeugende Belege geliefert.”

(1) Kwok CS et al. Int J Cardiol 2014;176: 680-686

Meat and cheese may be as bad for you as smoking

meat cheese

That chicken wing you’re eating could be as deadly as a cigarette. In a new study that tracked a large sample of adults for nearly two decades, researchers have found that eating a diet rich in animal proteins during middle age makes you four times more likely to die of cancer than someone with a low-protein diet—a mortality risk factor comparable to smoking.

“There’s a misconception that because we all eat, understanding nutrition is simple. But the question is not whether a certain diet allows you to do well for three days, but can it help you survive to be 100?” said corresponding author Valter Longo, the Edna M. Jones Professor of Biogerontology at the USC Davis School of Gerontology and director of the USC Longevity Institute.

Not only is excessive  consumption linked to a dramatic rise in cancer mortality, but middle-aged people who eat lots of proteins from animal sources—including meat, milk and cheese—are also more susceptible to early death in general, reveals the study to be published March 4 in Cell Metabolism. Protein-lovers were 74 percent more likely to die of any cause within the study period than their more low-protein counterparts. They were also several times more likely to die of diabetes. But how much protein we should eat has long been a controversial topic – muddled by the popularity of protein-heavy diets such as Paleo and Atkins. Before this study, researchers had never shown a definitive correlation between high  and . Continue reading

Why Artificial Sweetener Can Be Dangerous


When you buy a diet coke, or any other consumables containing the artificial sweetener aspartame, you’ll see a warning against consuming the product if you have phenylketonuria, an inherited metabolic disorder.

“Artificial” sweeteners, such as NutraSweet and Equal, are not saccharides – the simple carbohydrates we call sugars. Instead, the sweetener aspartame is a methyl ester 2comprising two joined amino acids: aspartic acid and phenylalanine (Phe) – this is important for later so keep it in mind. The safety of aspartame for general consumption has attracted attention since its discovery in 1965, but there’s no evidence of association with adverse effects. The warning on products containing aspartame is specifically for those with the severe disorder known as phenylketonuria.

Genetic basis

For someone to have phenylketonuria, they have to inherit an incorrect copy of a gene involved in Phe breakdown from each parent. Typically, the parents of an affected person (known as carriers) each have one correct and one incorrect copy of the gene, so are unaffected themselves. The main feature of the condition is the body’s inability to break down excess Phe (recall that this one of the two amino acids in aspartame). Now, this part gets complicated but stay with me.

Amino acids can join linearly and fold into three dimensional shapes to construct functional proteins that perform a wide range of roles in our bodies. We produce some amino acids ourselves, but others, including Phe, must be obtained directly from our diet. Amino acids can’t be stored by the body if we consume them in excess (unlike fats, for instance, and carbohydrates), so we need a constant supply. They also can’t be directly eliminated from the body, which means when excess amino acids are ingested, each type has to be broken down in a specific sequence of steps before excretion.

The first step in the degradation of Phe is its conversion to tyrosine, an amino acid important in neurotransmission (when signalling molecules from one neuron bind to and activate another). This reaction requires an enzyme as well as the assistance of a sidekick (enzyme co-factor). The enzyme is produced through expression of its corresponding gene, and a problem arises when there are mutations in this gene.

There are 548 separate mutations recorded for this gene that lead to the production of a differing enzyme, which means the body may not be able to break Phe down. This differing enzyme has a reduced ability of perform the initial step in the breakdown of Phe, so the level of the amino acid in the body rises. And this has a toxic effect on neurons. Early detection of high Phe levels and intervention is vital to avoid severe mental disability.

Diagnosis and treatment

Phenylketonuria was first identified by Asbjorn Folling, a biochemist and physician, who noticed an unusual odour in the urine of some individuals with developmental delays. This smell was due to a molecule produced by the body when Phe accumulates. A diagnostic test that worked reliably from around eight weeks of age (a drop of ferric copper added to a wet nappy would turn green in a positive test) was developed in the late 1950s. The problem was that, by this age, untreated babies had often already suffered brain damage.

Only a few years later, a new, more sensitive method permitted detection from three days after birth. The Guthrie or heel-prick test requires only a drop of blood from an infant. This blood is spotted on a paper disk and placed on growth media featuring bacteria unable to synthesise Phe. Growing bacteria – because the Phe present in the blood spot supplements what they are unable to produce themselves – represents a positive result. The heel-prick test is widely performed as part of neonatal screening programs. But the diagnostic test now uses a technique called tandemmass spectrometry and screening includes a wide range of conditions.

In the 1950s, a low-Phe diet was introduced for people with this severe metabolic disorder and it continues to be the predominant treatment. Since Phe is found in most food sources, the diet involves getting most energy intake from a formula instead of meals, supplemented by a small amount of foods low in protein (such as fruit and vegetables). The restrictive nature of this diet means researchers are still looking for better treatments avenues. A synthetic form of the enzyme co-factor is one option, as it an enzyme able to break down Phe and gene therapy.

But the reason why people with phenylketonuria can’t have aspartame-sweetened food is because, during digestion, it can separate into its component amino acids (aspartic acid and Phe). And this is bad news for people with the disorder.

Source: LiveScience