Garlic and Tomatoes

Garlic and Tomatoes

Maybe there’s a berry that tastes a little better? A research team funded by the Welch’s company tested Concord black grape juice in relation to BPH, but no benefit was found. If cranberries help best as fruit, what about vegetables? In see.nf/garlictomatoes I discuss trials with tomato paste and garlic extracts with respect to BPH. Unfortunately, in both cases these were before-and-after studies without control groups, which is why the purported benefits are only suggestive.

Maintaining Circulation

A famous 17th-century physician is said to have declared: “A man is as old as his arteries.” A woman too, even if most people don’t seem to realize that. In a nationally representative survey of American women, it turned out that most considered cancer to be their greatest personal health risk. Only 13 percent correctly named cardiovascular disease, the number one killer of women (and men and 100-year-olds). Unfortunately, the American Heart Association had to find in surveys between 2009 and 2019 that the number of women who understood that cardiovascular disease would be their most likely cause of death had suffered an “alarming decline.”

A recent editorial in the journal Aging Medicine wrote very poetically that “the blood vessel is the candle of life,” and boldly claimed: “All diseases come from the vessels.” There is even a microcirculation theory of aging that posits that the loss of blood vessel density with age—up to 50 percent in some tissues such as regions of the brain—contributes to organ damage because the removal of waste products and the delivery of oxygen and nutrients are hindered. You could say: What brings us blood brings us life.

How to Boost Your EPCs

How can we stay young at heart? The self-repair capacity of our blood vessels depends on endothelial precursor or progenitor cells, which arise from stem cells in the bone marrow to repair any holes in our endothelium, the innermost lining of the blood vessels that ensures that blood flows easily. See in see.nf./epc what these endothelial progenitor cells can do and what you can do to increase their number and activity, such as avoiding secondhand smoke and doing regular aerobic exercise, which is the first and crucial measure to prevent and treat the aging of the arteries. What can diet do here?

A randomized controlled trial showed that reducing saturated fat intake (especially butter) significantly increased the number of endothelial progenitor cells, and that fits with the findings of a study in baboons that showed that even a few weeks of a cholesterol- and fat-rich diet brings about a dramatic premature senescence of endothelial progenitor cells. Individual foods that increased circulating endothelial progenitor cells were berries, onions, and green tea, and eating a whole-food, plant-based diet not only increased the number of endothelial progenitor cells, but also improved their function, along with a drop in LDL cholesterol.

Normal Cholesterol Levels Are Deadly Cholesterol Levels

Scientific consensus panels already determined decades ago—“without any doubt”—that lowering LDL cholesterol reduces the risk of heart attack. Consistent evidence shows “unequivocally” that LDL cholesterol is behind our number one cause of death, namely heart disease. This evidence base includes hundreds of studies involving literally millions of people. In other words: “It’s the cholesterol, stupid,” as the editor-in-chief of the American Journal of Cardiology, William Clifford Roberts, quipped. His CV is more than 100 pages long, and he has published about 1700 articles in the peer-reviewed medical literature. True, there are at least ten conventional risk factors for atherosclerosis, but as Dr. Roberts notes, it takes only one for the disease to progress: elevated cholesterol. All other factors such as smoking, high blood pressure, diabetes, lack of exercise, and obesity only exacerbate the damage that high cholesterol causes.

“Ugh!”, you’re saying now, because you just got your blood test results and learned from your doctor that your cholesterol is “normal.” But hold on. In a society in which it’s normal to drop dead of a heart attack, a normal cholesterol level isn’t necessarily cause for celebration. Heart disease sits at the top of the list of causes of death for women and men, and we definitely don’t want normal cholesterol levels. We want optimal levels—and not “optimal” according to arbitrary lab standards, but optimal for human health.

Normal LDL cholesterol levels are associated with the buildup of atherosclerotic plaque deposits in the arteries, even in people with, by current standards, optimal risk factors: blood pressure under 120/80, normal blood sugar, and total cholesterol under 200. If you show up at your doctor’s office with numbers like that, they’ll hang a medal around your neck. But when the bodies of the patients with such good numbers were examined by ultrasound and CT scan, clearly visible atherosclerotic deposits were found in 38 percent. Maybe those numbers aren’t so optimal after all.

Maybe we should only describe an LDL cholesterol level as optimal when it no longer causes disease. (Crazy idea!) How can we find that out?

When more than 1000 men and women between 40 and 50 were examined, most with “normal” LDL levels under 130 quite clearly had atherosclerosis. No deposits were found only when the LDL level was at 50 or 60, coincidentally the level of most people before our diet became what it is today. The majority of the adult population worldwide had LDL levels of about 50 milligrams/deciliter. Because today we live in a society of sick people, their average values are considered normal. What we want is a cholesterol level that is normal for the human species, and that would have to be about 30–70 milligrams/deciliter (or 0,8–1,8 mmol/l).

Even if an LDL level in this range seems extremely low by modern American standards, that is exactly the normal range in people who live and eat what our ancestors were genetically adapted to over millions of years: a diet centered on whole plant foods. When you consider that the LDL level our bodies are designed for isn’t even half as high as today’s “normal,” it’s no wonder we’re being swept away by a pandemic of atherosclerotic heart disease.

Why is there a tendency in medicine to accept small changes in risk factors when the goal shouldn’t be merely to reduce risk, but to prevent deposits from forming at all? In that case, how low should we go?

A renowned professor of vascular biochemistry noted: “In light of the latest findings from trials investigating the benefits and risks of markedly lowering LDL levels, the answer to the question of how low we should go is quite simple: as low as possible!” However, it also depends on how we get there. Low levels may indeed be better, but if we lower LDL with medications, we have to balance the benefit against the risk of side effects.