Photo from April Pulley Sayre’s new book, Being Frog.
I came across this site on Consumer Reports which argues against use of the word “Natural” on food labels.
What does “Natural” mean? In July 2019, the Academy of Nutrition and Dietetics (formerly the American Dietetic Association) said this:
Currently, no formal definition for the use of “natural” on food labels has been issued by the U.S. Food and Drug Administration or U.S. Department of Agriculture.
“Natural” means nothing. Rather, it means whatever the food producer wants it to mean. To me, it falls into the same bucket as “wholesome.” Can you think of other terms?
An aside … That Consumer Reports’ site also said:
Consumers care a lot about how their food is produced, and they have some specific concerns. Based on the survey results, most told us that they want their food produced in an environmentally friendly way, and they look to labels for cues as they make their decisions. When purchasing food, they want to support local farmers. Their other concerns include finding food that’s locally produced. And most are even willing to pay more for food to ensure that it was produced in fair working conditions.
Tell me … what people are buying a loaf of bread or some pasta caring that it was made with wheat that was locally grown? Or a cup of coffee or tea? Are people not buying tomato sauce because it was produced in unfair working conditions? When people go to a restaurant, do they ask if their burger came from a local cow? I don’t know these people. Where are they? I’m not saying sustainably-raised food and fair working conditions aren’t the goal. They are. I’m saying that many people are not in a position to base their food buying decisions on these factors. This survey is not cross-sectionally representative.
Here’s a fairly recent review article on enlarged prostate (benign prostatic hyperplasia or BPH) and how diet affects it.
Benign Prostate Hyperplasia And Nutrition, European Society for Clinical Nutrition and Metabolism, August 2019
BPH is common:
About 75% of men >50 yr of age suffer from BPH related symptoms.
These include irritative voiding symptoms such as frequency, urgency and nocturia, and obstructive symptoms such as weak urinary stream, incomplete bladder emptying, straining to void, and an intermittent stream.
The article discussed possible causes of BPH, how the condition progresses, and what may contribute to that progression. Some contributing factors: inflammation, elevated estrogens, elevated insulin (and thus insulin resistance). Other elements of the metabolic syndrome are also associated, such as high blood pressure, excessive visceral fat, obesity, and high waist circumference.
Some diet-related things one can do to lessen symptoms:
- Engage in regular exercise (at least 5 days a week) of moderate or vigorous intensity. OK, not diet-related, but a biggie.
- Replace animal protein with vegetable protein. This was a biggie too. “A larger association of BPH has been reported with animal protein than vegetable protein.”
- Limit vegetable oils. “High consumption of unsaturated fatty acids may contribute to lipid peroxidation of the cell membrane and of the components and fluidity of cell membranes, which may affect 5-alpha-reductase activity.”
- Watch calories. “High energy intake may increase abdominal obesity and sympathetic nervous system activity, both of which may increase the risk of BPH. The activation of the sympathetic nervous system and the consequent activation of prostatic smooth muscles may lead to worsening of lower urinary tract symptoms.
- Eat soy. “Soy is an inhibitor of 5-alpha-reductase and a low-potency estrogen. Consumption of non-fermented soy products (tofu, soymilk, edamame) results in a decreased incidence of prostate cancer. Soy may block the receptor sites that the stronger estrogens use to increase the accumulation of DHT.”
- Reduce serum cholesterol. “Metabolites of cholesterol have been identified in the hyperplastic and cancerous prostate gland. Statins lower the risk of both BPH and prostate cancer.”
- Eat less cholesterol and saturated fat (animal foods). “Foods high in cholesterol and saturated fat are rich in arachidonic acid which is the main precursor of inflammation.”
- Reduce preformed long-chain omega-3 fatty acids such as EPA and DHA found in seafood, fish oil, and algal-based supplements. “A high intake of eicosapentanoic acid and docosahexanoic acid was associated with higher prevalence of BPH, lower urinary tract symptoms and BPH related surger. Their high degree of unsaturation promotes lipid peroxidation which in turn leads to an increase in 5a reductase and prostatic dihydrotestosterone, increasing epithelial and stromal growth.”
- Increase plant-based omega-3 fatty acids (vegetables, flax, chia). “[They] help to reduce the influence of prostaglandins and leukotrienes on the inflammatory component of BPH. Whole flaxseeds have the added benefit of lignan fibers, which help to bind estrogen in the gut and thus promote estrogen removal.”
- Eat onions and garlic. “A multitude of benefits have been linked to allium vegetables, namely favorable effects on cardiovascular disease, antiproliferative action on human cancers, and prevention of diseases associated with aging. Garlic and its constituents inhibit key enzymes involved in cholesterol and fatty acid synthesis (including steroid hormones associated with BPH).
- Zinc. The RDA for adult men is 11 mg. Make sure you’re getting it. “A decrease in zinc levels in plasma and prostate tissue in men with BPH (and prostate cancer) has been reported. Zinc supplementation resulted in a reduction of prostate size as well as symptoms of BPH. This may be attributed to blockade of 5-alpha-reductase and/or inhibition of prolactin, resulting in the decreased uptake of testosterone by the prostate and consequent conversion to dihydrotestosterone. It also inhibits the binding of androgens to their receptors in the prostate. Pumpkin seeds are a rich source of zinc, this may explain their potential therapeutic benefit for BPH. Excessive consumption of zinc (>100 mg/day) should be avoided as it may increase the risk of advanced prostate cancer.
- Minimize coffee. “Coffee can decrease zinc absorption by 50%. Caffeine stimulates the adrenergic nervous system (smooth muscles of the prostate) and may worsen BPH symptoms.
- Get some vitamin D. “An increased intake of vitamin D from diet and supplements has shown a correlation with a decrease in BPH prevalence. Vitamin D attaches to its receptors in the prostate and bladder and inhibits prostate growth, lowers excessive contractility, and reduces inflammation. It also has an inhibitory effect on the RhoA/ROCK pathway, along with cyclooxygenase-2 expression and prostaglandin E2 production in BPH stromal cells. Vitamin D analogues of up to 6000 IU/day have shown to decrease the prostate volume in BPH patients.”
I summarized the food-related therapies above. The article also discussed supplements, citing research which backed their effectiveness. I didn’t go into that here but am including part of a table, as a list. To the ones below add Urtica dioica (stinging nettle) which was also shown to be better than placebo.
Since saw palmetto seems to be a popular supplement for BPH, this is what it said:
Saw palmetto has three positive effects on the prostate gland: anti-androgenic, anti-proliferative, and anti-inflammatory . It is aweak inhibitor of 5-alpha-reductase. It also reduces the number of estrogen and androgen (DHT) receptors. Saw palmetto inhibits fibroblast growth factor and epidermal growth factor, and stimulates apoptosis thus further slowing prostate cell proliferation. Its principle ingredient, beta-sitosterol, is also found in soy products (see above), as well as in other herbs used to treat diseases of the prostate including pygeum bark, stinging nettle root, and pumpkin seed extract. Saw palmetto has not shown any benefit in reducing the size of prostate. However, it has been found to improve symptom scores, nocturia, residual urine volume, and urinary flow in patients with BPH.
Altering the progression of BPH by lifestyle modification, dietary changes or supplementation with nutritional supplements is long known but not widely adapted. Performing moderate exercise 4 to 6 times a week, following a diet rich in vegetable protein and low in animal protein, fortification of diet with zinc and Vitamin D rich foods and intake of supplements like Saw palmetto, Cemilton and Pygeum extracts may help in controlling prostate growth and related LUTS [lower urinary tract symptoms].
There is a lot one can do, short of taking a pharmaceutical drug, to lessen BPH symptoms.
Great video by Dr. Klaper. To sum: no need for vegans to take DHA supplements. (More than no need, it’s probably not a good idea.)
I can’t seem to find just a simple loaf of bread out there … flour, yeast, and salt. So, for my regular daily bread I’ve been making this. It’s a half-wheat, half-white, no-knead bread. The overnight rise takes the place of kneading.
1.5 cups whole wheat flour
1.5 cups white, all purpose flour
1.5 cups water (plus up to 1/4 cup more)
2 teaspoons salt
1/8 teaspoon instant yeast
1 heaping teaspoon sourdough starter (optional)
- Stir salt and instant yeast into flours in a large bowl (it’s going to expand).
- Dissolve starter into the 1.5 cups water. Add to dry. Add up to 1/4 cup more if dough seems too dry. I always add it.)
- Cover with plastic wrap and a towel. Let rise 12 to 18 hours.
- Place dutch oven with lid into oven. Preheat to 500 degrees F.
- Sprinkle a few tablespoons of flour onto counter. Using a flexible spatula, nudge dough onto flour.
- Flour hands and pat some flour onto dough. Using pastry scraper, knead dough 5 or 6 times so it comes together into a loaf. Cover with plastic. Let rest 20 minutes while you line a cookie sheet with parchment paper.
- Using scraper, form dough into loaf (will take another 6 or so kneads). Transfer loaf to parchment-lined cookie sheet. Cover with plastic. Let rise 1.5 hours. If it starts to split or if a poked indentation doesn’t fill in, it’s ready to bake.
- Remove pot from oven. Score top of loaf. Lift with parchment paper and lower into pot (paper goes into pot with bread). Cover. Bake at 500 degrees for 30 minutes. Remove lid. Lower temperature to 470. Bake another 20 minutes.
How much DHA (docosahexaenoic acid, a long-chain omega-3 fatty acid) does the human body make? It depends. It’s not correct to claim a flat rate, say 1% or 10% or 15% of short-chain omega-3 gets converted to longer chain omega-3s like DHA. Each person is different. Even within a person, that rate changes. One variable that affects the rate is how much fat we eat.
This next study compared the effect of a low-fat diet (20% energy) to a high-fat diet (45% energy) on type of fats in the blood. The diets had the same calories and the same proportions of fatty acids (1:1:1 for poly:mono:sat). Designing these diets was a challenge.
Total Fat Intake Modifies Plasma Fatty Acid Composition in Humans, The Journal of Nutrition, February 2001
It was a crossover design, so participants ate one diet for a month, then their usual diet for a month as a wash-out, then the other diet for a month.
When they ate the low-fat diet, they had higher levels of omega-3 (n-3) fatty acids and lower levels of omega-6 fatty acids in their blood compared to the high-fat diet. Specifically, for example, compared to eating a high-fat diet, eating a low fat diet resulted in almost 30% more DHA in phospholipid fatty acids and 36% more DHA in cholesteryl esters.
The low fat diet was associated with significantly greater total (n-3) fatty acids, 20:5(n-3) and 22:6(n-3) levels in plasma phospholipid fatty acids and cholesteryl esters.
Eicosapentaenoic acid or EPA is 20:5(n-3) and docosahexaenoic acid or DHA is 22:6(n-3).
The consumption of a low fat diet promotes an increase in the level of total and highly unsaturated long-chain (n-3) fatty acids (>C20) and a decrease in the total (n-6) content of plasma phospholipid and cholesteryl ester fatty acids. The observed modifications in phospholipid and cholesteryl ester fatty acids in response to a low fat diet are similar to those observed when (n-3) fatty acids of plant or animal origin are fed. This may explain some of the beneficial effects of low fat diets.
How can you end up with higher amounts of EPA and DHA, if you’re not actually eating them?
This change is likely related to decreased competition for the enzymes of elongation and desaturation, with reduced total intake of 18:2(n-6) favoring elongation and desaturation of available (n-3) fatty acids.
What I didn’t realize about this study the first time I read it was that the high-fat group consumed MORE PREFORMED DHA than the low-fat group. They ate more fish. But they ended up with LESS DHA in blood.
Recall that this was a crossover design. So the same person’s conversion rate changed depending on how much fat they ate. You can’t just say 1% or 15% conversion; the background diet matters.
It doesn’t make sense to me that we would need to supplement with something the body produces, unless we are somehow thwarting that production.
The paper above was in 2001. Here’s a more recent review that continues to say:
In conclusion, while the current data support the suggestion that n-3 LCPUFA status in humans can be increased in the absence of increased n-3 LCPUFA intake, there is a need for well-controlled and adequately powered studies in males and females in order to evaluate whether these diets could be a viable alternative to n-3 LCPUFA supplementation for achieving improvements in human health.
– The effect of modifying dietary LA and ALA intakes on omega-3 long chain polyunsaturated fatty acid (n-3 LCPUFA) status in human adults: A systematic review and commentary, Prostaglandins, Leukotrienes and Essential Fatty Acids, April 2015
The study at the top was small (although well-controlled: food was provided, dinners served in metabolic ward, it was cross-over with wash-out periods) and it mixed men and women of a broad age range (22 to 65 years old). There was 100% retention, everyone finished the study. To scale this up would be an enormous expense – an investment, I imagine, that would not be returned since the intervention requires doing less of something: eating less fat, especially the type (omega-6) that our diets are flush with from all the subsidized corn and soy oils we eat. If it’s not a pill, drug companies won’t pay for it, and drug companies pretty much own academic and government research these days. The agricultural industry, producers of all our omega-6, would likely also discourage it.
Let’s look at a 10% conversion rate…
There are about 3 grams of ALA in 7 walnut halves and 1 tablespoon of ground flax seeds. If our livers converted 10% of that 3 grams to DHA (assuming a whole lot of things but this is hypothetical), that’s 300 mg. And most plant foods contain ALA so it’s likely we get more than 3 grams a day. That 300 mg DHA is more than the 250 mg Dr. Greger advises taking in an expensive, partly-oxidized, ultra-processed, algal-derived omega-3 pill.
There’s also this:
“The best conversion rates [of ALA to EPA and DHA] are by individuals that don’t consume DHA and EPA.”
Omega-3: ALA intakes enough for EPA/DHA levels for non-fish eaters?
I’m happy to see there’s something people can do besides taking a pill: Eat a low-fat diet.
Dr. Greger has been telling his readers to consume DHA (Docosahexaenoic acid), a type of omega-3 fatty acid obtained mostly from seafood. But seafood is some of the dirtiest food you can eat. So, he advises getting DHA from algae. Problem is, algae-derived DHA, in the amounts he recommends (250 mg/d) can only realistically be supplied in supplement form. Why is that a problem? It’s an extract, not a whole food; it’s ultra-processed; its production is energy-intensive; its often more oxidized/rancid that seafood-derived DHA; and the limiting factor for most people: it’s expensive. (Nordic Naturals cost $25 for a 30-day supply. That’s $100 for a family of 4, on top of their regular food budget. For life.)
The algae has to be grown, either inside in climate-controlled laboratories or outside in ponds. Farming algae (including feeding), harvesting and extracting its oil, discarding or repurposing the remainder, and packaging the purported valuable bit in single-serve capsules requires lots of energy. All told, eating algal DHA could be worse for the environment than eating seafood.
Do we even need to eat seafood or algae oil at all? John Langdon argues that we don’t:
A number of authors have argued that only an aquatic-based diet can provide the necessary quantity of DHA to support the human brain. … There is no evidence that human diets based on terrestrial food chains … fail to provide adequate levels of DHA or other n-3 fatty acids. Consequently, the hypothesis that DHA has been a limiting resource in human brain evolution must be considered to be unsupported.
– Has An Aquatic Diet Been Necessary For Hominin Brain Evolution And Functional Development?, John Langdon, British Journal of Nutrition, 2006
Dr. Greger is saying that everyone should take algal DHA supplements, not just vegans, because omnivores have an “omega-3 index” that’s “just as bad” as vegans.
Millions of people cannot afford to take algal supplements for the rest of their lives. But many will think they need to, to get the long-chain omega-3 fatty acid DHA. What will they do? Eat seafood.
I’ll use canned tuna as an example but my arguments apply to most seafood. … The 5 ounce can of tuna fish below costs about $0.76 on Amazon. It contains about 300 mg DHA, 20 grams of protein, and can provide the basis of a meal for 2 or more people. Unfortunately, it also contains pollutants from the water in which it lived: pesticides, flame retardants, polychlorinated biphenyls (PCBs), mercury, arsenic, lead, and other heavy metals, pharmaceuticals, teflon, microplastics. Tuna are being fished at unsustainable rates and there’s no such thing as a “dolphin-friendly” catch. Also, tuna and other fish are intelligent: “Science has shown fish to be capable of collaboration, recognition, astonishing feats of memorization, and craving physical touch.” There are so many reasons not to eat tuna fish. But many people will not get past my first two sentences.
There isn’t an RDA for DHA because the Institute of Medicine says it’s not an essential nutrient, meaning we don’t have to consume it because our bodies make it. We make it from ALA (alpha-linolenic acid) an omega-3 fatty acid that’s found in lots of plant foods (like flax, walnuts, kidney beans, oatmeal, cauliflower, spinach). One way we can make more DHA is to reduce the amount of omega-6 fatty acid in our diet (from vegetables oils like soy), or just eat a low-fat diet. That reduces competition for the converting enzyme (my second reference below).
Here are some of my past posts on this topic:
The Forgotten Art Of Squatting Is A Revelation For Bodies Ruined By Sitting, Rosie Spinks, Quartz, 9 November 2017
This devotion to placing our backsides in chairs makes us an outlier, both globally and historically. In the past half century, epidemiologists have been forced to shift how they study movement patterns. In modern times, the sheer amount of sitting we do is a separate problem from the amount of exercise we get.
Squatting isn’t just an artifact of our evolutionary history. A large swath of the planet’s population still does it on a daily basis, whether to rest, to pray, to cook, to share a meal, or to use the toilet.
Deep squatting as a form of active rest is built in to both our evolutionary and developmental past: It’s not that you can’t comfortably sit in a deep squat, it’s just that you’ve forgotten how.
Our failure to squat has biomechanical and physiological implications. … “Every joint in our body has synovial fluid in it. This is the oil in our body that provides nutrition to the cartilage,” Jam says. “Two things are required to produce that fluid: movement and compression. So if a joint doesn’t go through its full range—if the hips and knees never go past 90 degrees—the body says ‘I’m not being used’ and starts to degenerate and stops the production of synovial fluid.”
Studies show that greater hip flexion in this pose is correlated with less strain when relieving oneself. … Indeed the realization that squatting leads to better bowel movements has fueled the cult-like popularity of the Lillipad and the Squatty Potty.
I get the feeling that if you haven’t squatted for most of your life, it’s not going to be an easy posture to assume. Still, we really should be squatting more.
I welcome you to enjoy this photo of a squatting Safika Lemur as much as I did.