As men age and fat surrounding their internal organs accumulates, the risk of prostate cancer rises—a link doctors are unlikely to mention. Tony Edwards reports
I recently lost two friends to prostate cancer. They were in their 70s and had apparently lived healthy lives, but they were mercilessly dispatched by men’s most common cancer.
Although my pals had been slim and athletic in their youth, in their 50s they began to get a bit portly—their bellies in particular were making them appear to be in an advanced state of pregnancy, with the classic taut skin stretched over the abdomen. Not a good look and, as it turns out, a bad look-out for their health.
Recently, English TV personality Jeremy Clarkson announced that he, too, had been diagnosed with the cancer. And Clarkson’s Farm fans around the world couldn’t have failed to notice that he, too, was developing a bit of a bulge in the midriff.
“The poor man looks six months pregnant,” my female friends jocularly observed. But Clarkson and my two deceased chums raise a serious question: Is there a connection between these three men’s bellies and their prostate cancer diagnosis?
In a word, the firm answer is yes. But the scandal is that medical advice to men has been largely silent on the matter.
The prostate is a uniquely male organ which surrounds the urethra (urinary tract) shortly after it exits the bladder. It’s usually described as the size and shape of a walnut.
This gland plays a correspondingly minor role in the body: It adds some carrier fluid to sperm and pumps the resultant liquid through the erect penis during the few seconds of sexual orgasm. You could be forgiven for concluding that for 99.9 percent of a man’s lifetime, the prostate doesn’t seem to do much.
But not so. When apparently lying inert astride the urethra, the prostate is quietly at work, spending every hour of every day doing two jobs: building up a reservoir of sperm carrier fluid and seeping natural chemicals into the urethra to prevent infection. Both of these jobs depend on a souped-up version of the hormone testosterone to “unlock” key contents of the prostate, such as zinc, proteins, enzymes and antimicrobials.
But here’s the problem: This souped-up substance is dihydrotestosterone (DHT), a potentially nasty chemical despite its natural origin. Its most obvious toxic action is to destroy hair follicles, causing baldness in over 80 percent of men.
DHT also creates skin conditions such as acne. But its most toxic effect is on the prostate itself. Astonishingly, the very compound which the prostate itself manufactures is potentially suicidal.
How? It turns out that year-in, year-out manufacture of DHT finally exhausts the organ. It keeps on producing new prostate cells but “forgets” to remove the dead ones. This inevitably causes the prostate to enlarge, a condition which medics call benign prostatic hyperplasia (BPH).
The inescapable truth is this: Whether you believe in creationism, intelligent design or random evolution, the entity which created the prostate seems to have done a pretty crummy job of it. Half of men over age 50 and all men over age 90 develop BPH of various degrees of severity.
Its range of symptoms includes weak urine flow, frequent voiding and urine retention—occasionally even total retention. Those unpleasant or even life-threatening side effects and male baldness are two major downsides of DHT. Indeed, if Mother Nature were a pharma company and wanted to market DHT as a powerful aid to male fertility (which it clearly is), the regulators would probably give it a thumbs-down on its side effects alone.
But what about prostate cancer? Can DHT be responsible for that, too? Big Pharma certainly thinks so and has developed a range of drugs to attack it; these anti-androgen drugs are used to both prevent and treat prostate cancer.
But do they work? Yes and no. For example, anti-androgens such as finasteride overall reduce the risk of prostate cancer by about 30 percent, but they can also cause more aggressive cancers in many men. And they have little or no effect on death rates.1
As for treating prostate cancer itself, again men have been let down by Big Pharma, as a recent survey admits. Regarding androgen deprivation therapy (ADT), the first-line approach to metastatic prostate cancer, it notes that “although ADT initially induces clinical regression, most tumors eventually evolve resistance and progress to lethal castration-resistant prostate cancer.”2
Earlier this year, Jeremy Clarkson was diagnosed with “aggressive” early-stage prostate cancer; lucky for him, an MRI showed that only about 10 percent of his prostate was affected. He opted for one of the latest techniques for removing it—not invasive surgery but targeted sound waves.
In high-intensity focused ultrasound (HIFU), sound waves are focused on the problem areas of the prostate; these raise the temperature of the diseased tissue and destroy it. But such prostate cooking comes at a price—about £15,000 ($25,000).
That’s what men may need to pay to avoid the side effects of surgery, mainly incontinence and erectile dysfunction, as HIFU is neither offered by the National Health Service nor covered by health insurance. Also available only if you pay for it is the advanced diagnostic test used by Clarkson’s doctors (see below).
However, the main question is this: Did Clarkson’s “six months pregnant” embonpoint cause his prostate cancer? The answer may depend entirely on the type of extra abdominal fat he carries.
There are two kinds of belly fat. One is superficial fat, technically known as subcutaneous adipose tissue or SAT, which is the wobbly flesh you can clench with a hand. Surface fat may be unsightly, but it’s not particularly unhealthy.
The second type is visceral fat (VAT), which accumulates deep in the torso, surrounding major organs such as the intestines, pancreas, liver, kidneys, heart and even the prostate itself. It’s VAT which causes the taut belly skin, making a man look pregnant.
Men are particularly prone to store visceral fat. One theory says it’s all down to our hunter-gatherer past. During long hunting trips on the savannah, VAT is a better source of stored energy than SAT.
That was all very well when life expectancy was around 35 years, but the problem is, at almost exactly that age, modern man hits the male menopause. It’s not as sudden or severe as the female one but is arguably more self-destructive. For, as a man’s testosterone levels drop (by 1–2 percent every year), that sets in train a doom loop.
In men’s youth, testosterone prevents fat storage, but the midlife drop in testosterone levels means less fat inhibition and hence more fat cells. Those cells also contain a feminizing enzyme called aromatase, which converts testosterone into estrogen, which then attacks testosterone, accelerating its natural decline, which in turn promotes further fat storage. It’s a truly vicious cycle which seems to make a VAT belly almost inevitable.
Fortunately, not all men are affected, mainly due to luck (genes) but also to lifestyle (see below).
For men with VAT bellies, later in life another doom loop occurs, leading to prostate cancer. Unlike superficial belly fat, visceral fat is not an inert energy storage mass.
It functions like an endocrine organ, pumping out pro-inflammatory cytokines and aromatase, once again destroying testosterone. Then it releases chemicals that cause insulin resistance. They also raise leptin, promoting cell division, and suppress adiponectin, which is a natural anticancer agent.
The mechanism is so coherent that it’s almost elegant: Visceral fat leads to chronic inflammation and hormonal disruption, which leads to an aggressive tumor-generating environment.
The epidemiological evidence is pretty clear, although it’s taken medicine some time to cotton on. It was only as recently as 20 years ago that researchers first established (via detailed abdominal measurements) that men with VAT have six times extra risk of prostate cancer.3
But is that a sentence of death? No. A sixfold increase in risk is on the moderate-to-high scale, meaning some VAT men will either have low-grade prostate cancer or escape it altogether. Indeed, most men die with prostate cancer rather than of it.
Nevertheless, the more VAT, the greater the prostate cancer risk. So, if a man starts to look pregnant, he and his loved ones shouldn’t ignore it.
His doctor probably will, though. Astonishingly, family doctors on both sides of the Atlantic have been told to ignore the belly–prostate cancer connection. While there’s some screening in the US, doctors in the UK have been told to wait until the telltale urinary symptoms occur.
The best preventive strategy for VAT is the bog-standard duo of diet and exercise.
Remarkably, Jeremy Clarkson seems to have got the message, announcing that he’s intending to do “more walking,” cut out processed foods and even become more vegetarian. But sadly, little of that will cut the mustard with VAT. So what should he, and other men, do instead?
Exercise
A surprising number of research studies have investigated exercise regimes specifically targeting visceral fat. Understandably, their findings have not been 100 percent consistent, but a recent meta-analysis synthesized the data, concluding that the two best exercise regimes are vigorous-intensity aerobic exercise and high-intensity interval training.4
In practical terms, both amount to the same thing: tough, exhausting workouts (minimum 30 minutes long, three times a week for three months). So mere walking doesn’t come close, Jeremy.
A far less onerous option is dietary changes.
Diet
Here, too, medical science has been remarkably active. Unsurprisingly, the core food regime has been found to be the Mediterranean diet, widely considered the world’s healthiest diet. It features fruits and vegetables, olive oil, more fish than red meat, whole-grain foods, eggs, yogurt and red wine with meals.
But Harvard nutritionists have gone a step further by bolstering it with three extra ingredients: walnuts, green tea and a green alga called Mankai. Remarkably, these additions make the Med diet twice as effective at reducing visceral fat.5
Intermittent fasting also delivers powerful results—particularly the 16:8 protocol of a daily 16-hour fast. The easiest way to achieve this is to skip breakfast and eat lunch and dinner within an eight-hour window. Even more effective is to eat earlier in the day (such as from 8 a.m. to 4 p.m.) and avoid food in the evening, which better matches the circadian rhythm and is shown to be associated with a lower weight.6
Because visceral fat is metabolically intensely active, the body chooses it as the main fuel source during the 16-hour energy shortfall. This has been dramatically confirmed in numerous studies, most of which have seen a “considerable decrease” in VAT after adopting a 16:8 diet regime, even after as little as 12 weeks.7
But Clarkson’s doctors may well have recommended the quick fix of a “fat jab.” Injections such as Ozempic, Wegovy and Mounjaro do indeed result in dramatic reductions in VAT, but often at a cost to long-term health.
Those who take them often become protein-deficient and tend to lack micronutrients such as vitamin D, iron, calcium and vitamin B2 (thiamine); these are “meaningful nutritional deficiencies,” say researchers.8
In an effort to prevent another type of deficiency, in 1998, the United States mandated the fortification of American flour with folic acid, the synthetic form of folate (vitamin B9). This was done to prevent neural tube defects such as spina bifida in newborn babies (see below).
The UK is about to follow suit. In December, Brits will also be mass-medicated with folic acid when it becomes compulsory for manufacturers to add it to white flour.
But what’s the prostate connection? Folic acid supplementation can increase the risk by up to 25 percent.9
Powerful confirmation has come from laboratory tests. When folic acid is added to prostate cancer cell lines, cancer “growth and invasion” is markedly increased. “Folic acid has an important and potentially negative role in prostate cancer progression,” say Canadian researchers.10
But, while folic acid is carcinogenic, natural folate is not. This was recently demonstrated in a survey of about a quarter of a million men taking part in the UK Biobank study.11
Folate itself is important for brain and heart health. It’s found in dark green leafy vegetables, legumes and organ meats like liver and is also available as a food supplement.
You might wonder, if it has already been made into a pill, that means it started out as a powder. So if the authorities are keen on reducing neural tube defects, why don’t they fortify flour with harmless folate powder rather than with potentially risky folic acid?
Their answer is that folic acid is more stable and is less degraded by cooking. But there’s another reason: Folic acid is much cheaper than folate. The die is cast, however. No ifs or buts. Folic acid is being added to flour whether you like it or not.
What should men do in the face of this potential threat to their health?
Option one is to keep calm and carry on. After all, say the US authorities, the amounts of folic acid are too low to have any adverse effects. As proof, they point to the raw figures: There has been no uptick in prostate cancer cases since their policy came into effect over 20 years ago. Case closed.
On the other hand, there is still uncertainty in the basic science. Researchers admit they haven’t much of a clue why folic acid can cause the cancer. In the face of such ignorance, surely the wisest course of action is the precautionary principle: Governments shouldn’t meddle with human biochemistry if they don’t fully understand it.
Option two is to avoid foods made with refined flour. To reduce public backlash, the US and UK authorities have exempted whole-wheat products from fortification—a prudent diplomatic move with the benefit of encouraging healthier food choices.
On the face of it, it might seem absurd to subject millions of men to an extra risk of cancer—however small—to possibly prevent a few hundred neural tube defect cases a year in British and American neonates. Ironically, the link between folic acid and birth defects was once so controversial that the Briton who first proposed it, Professor Richard Smithells (1924–2002), was almost hounded out of the medical profession.
In the 1970s and 1980s, the theory that a mere vitamin deficiency during pregnancy might cause such serious outcomes was widely ridiculed, and Smithell’s attempts to prove it in clinical trials were actually blocked by officialdom. Finally, however, the forces of ideological censorship were vanquished and the importance of maternal nutrition established.
But does mass folic acid medication work? Despite its enthusiasm, the US Food and Drug Administration admits that the policy doesn’t prevent most neural tube defects, possibly because of the relatively low level of fortification (140 mg per 100 g of flour, increasing mothers’ intake by a mere 0.1 mg a day). The UK government projects a similarly poor outcome, expecting that 80 percent of these defects will still occur despite almost double the fortification rate.
Why haven’t the folic acid levels been raised to actually produce the intended outcome? Because of “safety concerns,” say governments. One of their top concerns is prostate cancer since the evidence is so clear that folic acid is bad news for prostates. For example, a 10-year study found that regular users of folic acid had a three times higher risk of prostate cancer than non-users.1
In addition to lifestyle changes, what can men do to prevent prostate cancer? There are three main non-pharma solutions with good track records.
Saw palmetto. This American plant of the palm family is packed full of compounds which antagonize DHT. They have shown efficacy in both preventing and managing symptoms of BPH as well as, to a certain extent, prostate cancer itself.
However, initial clinical trials have had mixed results, and only supplements containing consistently high levels of the plant’s key ingredient—beta-sitosterol—have produced reliable benefits.1
Suggested dosage: 320 mg daily saw palmetto extract has been used in studies of BPH; 60–130 mg daily beta-sitosterol is usually used for general prostate health
Lycopene. Extensive laboratory and clinical trials of this natural plant compound found in red and yellow fruits and vegetables, particularly tomatoes, have shown that it can “effectively suppress the progression and proliferation” of prostate cancer.2
Lycopene is preferentially absorbed by the prostate, where it has multiple beneficial effects. It’s antioxidant and anti-inflammatory, interferes with the growth and spread of cancer cells, and induces apoptosis (programmed cancer cell death).3
However, to obtain lycopene’s full benefits, tomatoes must be cooked. That releases four times more lycopene than from raw tomatoes. The most concentrated source is tomato paste.
Suggested dosage: 10–30 mg daily
Zinc. This mineral is concentrated in the prostate and is a vital part of its health. Indeed, zinc deficiency is closely linked to an increased risk of prostate cancer. Long-term use of zinc supplements results in a 66 percent reduction in the risk of advanced prostate cancer. Higher doses appear to be counterproductive, however.4
Suggested dosage: 15–25 mg daily
Can sexual inactivity lead to prostate cancer? There’s no consensus on the answer; views differ among researchers. On the one hand, Harvard’s 18-year study of 31,000 men found that those who ejaculated at least 21 times a month had a modestly (20 percent) reduced risk of prostate cancer compared to less active men.1
But other studies have not been so positive, possibly because it’s inherently difficult to obtain reliable data. In theory, however, it’s believed that “frequent prostatic flushing” should create a healthy microbial environment hostile to cancer.
For years, the primary screening tool for prostate cancer has been to measure blood levels of prostate-specific antigen (PSA), a protein produced by both normal and malignant cells in the prostate. High levels are thought to indicate the presence of the cancer.
But the test is beset with problems. All it really indicates is extra prostate activity, which could be caused by mild inflammation and BPH as well as cancer. It’s no surprise that about 75 percent of men with elevated PSA levels are found not to have cancer when biopsy samples are actually tested.
And biopsies themselves are no walk in the park: A needle inserted between the anus and the scrotum is quite painful despite sedation. What’s more, up to 30 percent of biopsies may actually miss a cancer or mistake a low-grade cancer for an aggressive one. So some men may undergo multiple biopsies before receiving an accurate diagnosis.
That poor track record has led urologists to demand better detection methods, such as the use of MRI—getting actual pictures of the prostate. These are quite good at finding diseased tissue, but such advanced technology comes at a price.
In fact, MRI is now increasingly used in conjunction with a new screening test recently developed at Sweden’s prestigious Karolinska Institute. Dubbed Stockholm3, it differs markedly from the standard PSA test by using multiple prostate fluid markers rather than just one and taking a full patient clinical history.
But its major breakthrough is doing DNA tests to look for genetic variants associated with prostate cancer. The result produces a personalized risk profile that is far more accurate than PSA alone, particularly for detecting aggressive cancers. Results are an impressive 90 percent detection rate—twice that of a PSA test.1
At present, men in the UK must pay out of pocket to obtain Stockholm3, and it typically costs £350–£500. Pricing has not been established in the US, where the test is undergoing trials but has not yet been approved by regulators.
In the United States, PSA-only screening is offered to men in their 50s, and to African-heritage men in their 40s (because Black men have a genetic fourfold extra prostate cancer risk). The UK has no screening program whatsoever. However, both countries agree that men over age 70 should not be screened because the harms of prostate cancer treatment outweigh the benefits for those with limited life expectancies.
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