As you know, I regularly scour the health and medical news to bring you a common sense analysis of what’s really going on. Here are three of my latest finds.
Which diet is best for metabolism?
When it comes to weight loss, there are many studies attempting head-to-head comparisons of various diets, typically ultra-low-fat “plant-forward” DASH diets vs. Mediterranean diets replete with fresh fruits, vegetables, fish, olive oil, whole grains and some red wine, vs. Atkins-style very low-carb keto diets that deliver fat and protein.
Results vary, but most studies arrive at a consensus: Any diet that interposes a barrier between the dieter and the refrigerator will produce weight loss. Results are generally comparable.
That, too, is the conclusion of a recent study that examined not just weight loss, but the metabolic consequences of each of the three popular diet paradigms for a specific type of dieter: Overweight middle-aged individuals with borderline or elevated blood sugar and fatty liver.
Metabolism vs. pounds
A very high percentage of Americans fit this pattern—metabolic syndrome. In the U.S., about 1 in 3 adults has metabolic syndrome, and its incidence increases with age. It’s a major driver of preventable chronic disease.
Conceding that the ship has sailed on the question of which diet is the best for losing weight—indeed all three groups of dieters in the trial lost roughly comparable pounds—the researchers focused on blood sugar and fat accumulation in the liver.
Insulin sensitivity improved among adherents to all three diets—but was two to three times better with the keto diet. Moreover, the keto diet improved 24-hour blood glucose measurements by 20% compared to merely 8% on the other diets.
The fatty diet that makes liver fat disappear
Think all that fat in the keto diet would end up in the livers of experimental subjects?
Au contraire! While losing weight helped all three diet groups shed liver fat, the keto diet reduced fat inside the liver by 67% compared to 45% for the other two diets after five months.
This study has clear implications for people who are overweight—an estimated 75% of whom have excess fat accumulation in the liver, which has surpassed alcoholism as the major cause of liver cirrhosis necessitating liver transplantation.
The researchers also propose that more research be undertaken examining the potential beneficial synergy that could be achieved by teaming low-carb keto diets with popular GLP-1 weight loss drugs.
It’s not just about losing weight—it’s how you get there.
“My doctor told me that everyone over the age of 70 should be on a statin”
That was from a listener who called into my radio show last weekend.
It’s true that cardiovascular disease is the major cause of death in the U.S.—1/3 of people die from heart disease or stroke.
But that also means two-thirds of people die from other causes—cancer, Alzheimer’s, myriad other causes, or simply old age. And of those who do die of cardiovascular disease, a third of them don’t make it to 70.
The controversy
Until recently, there was considerable debate over the value of statins for people over 70 for primary prevention—forestalling problems in seniors with no prior diagnosis of cardiovascular disease. Scores of older adults would have to be treated unnecessarily to stave off just one cardiac event.
On the other hand, just as in younger people who’ve had a heart attack, suffer angina, have needed bypass surgery or a stent, or have multiple risk factors like obesity, hypertension, high cholesterol or lp(a), or diabetes, there is good rationale to continue statins past 70—especially now that with modern medical advances it’s not uncommon for people over 70 to enjoy a decade or two of additional longevity. No longer are septuagenarians simply “written off”.
A lucrative new market for statins?
But lately, due to “diagnostic creep”, —i.e. expanding markets to sell more medicines—there’s been an effort to extend the supposed preventive benefits of statins to otherwise healthy seniors.
This was supported by a 2024 study. Researchers from the University of Oxford found statin treatment was both “cost-effective and correlated to better health outcomes in older adults with or without previous cardiovascular disease.”
A more recent study found that Lipitor at a high dose of 40 mg per day reduced cardiovascular events in seniors without pre-existing risk factors by 30%. It was hailed as “the first large-scale trial of a statin for primary prevention to show cardiovascular benefit in people aged 70 years and older.
That’s probably where that doctor got their latest marching orders—statins for all seniors, no exceptions!
Doubts linger . . .
Here’s the rub: In this same trial, it was found there was no impact on dementia risk or disability-free survival. In other words, in the long run, statins made little difference for the ultimate outcome—whether seniors lived longer, free of handicaps.
Moreover, a recent study found that over-75s who had been taking statins—30% of whom had diabetes and 77% hypertension—could safely discontinue them with no adverse consequences. The rate of adverse events was the same for them as for the control group who stayed on their statins—even when their cholesterols surged to an average 257 mg/dl!
That’s why discretion should be exercised when prescribing statins to seniors. While statin foes exaggerate their harms, they can cause side effects, including muscle aches, weakness or fatigue, cognitive problems, and elevated blood sugar. When risk is minimal to otherwise healthy seniors, why go there?
A better way
A helpful tie-breaker test is the coronary artery calcium score, which assesses the degree of plaque accumulation in the coronary arteries. If it can be demonstrated that a senior has a zero or minimal score at 70, it’s passingly rare for them to accumulate sufficient additional plaque in the years remaining to them to be of any consequence.
Now at 73, with a zero score a few years back, I’ve made the decision to forego statins.
The blanket statement that everyone over 70 should take a statin “just in case” is at best misinformed, and lacks nuance and individualization; at worst, it’s a form of “medical gaslighting” to intimidate patients into complying.
The persistent challenge of lipoprotein(a)
Followers of Intelligent Medicine are familiar with my frequent discussions about lp(a), a newly-recognized cardiovascular risk factor. I’ve been predicting that before long, people with high lp(a) will be able to take revolutionary new drugs to lower it.
It turns out, not so fast!
What’s lp(a)?
Lp(a), like LDL cholesterol, is a particle carried in the blood stream. But unlike cholesterol particles, it’s not amenable to diet change or exercise, and statin drugs don’t budge it. It’s mostly genetically determined.
When people with seemingly normal cholesterol have heart attacks, lp(a) may be the hidden culprit.
Newer PCSK-9 drugs may lower lp(a) 20-30%, but that may not be enough to substantially lower cardiovascular risk.
It’s now recommended that everyone get an lp(a) test just once; repeat tests don’t make much sense, until the advent of effective drugs to slash it.
Drug companies are working overtime, and investing billions of dollars, to develop novel drugs to tackle lp(a), anticipating lucrative returns.
Another BigPharma fail?
But last week it was revealed that a promising Novartis candidate drug—pelacarsen—while succeeding in slashing lp(a) by 80%, didn’t reduce the risks of cardiovascular disease—deaths, heart attacks and strokes—compared to placebo.
The news took Novartis stock from a high of 160 to a low of 137. Other companies with lp(a) lowering drug candidates in their development pipelines are expressing similar consternation.
Researchers are puzzled as to what happened. Of course, there are precedents for other promising approaches to cardiovascular prevention that seemed plausible but failed “where the rubber meets the road”.
It was once thought that high-dose niacin, with its propensity to lower total cholesterol, while raising “good” HDL, was an ideal preventive. But it crashed and burned after clinical trials showed it had no impact on actual outcomes.
BigPharma giants later undertook a fruitless quest to develop HDL-boosting drugs; while high HDL is generally protective against cardiovascular disease, raising it artificially didn’t confer benefits. The dead end was a multi-billion-dollar write-off for drug makers.
Back to the drawing board?
Why didn’t pelacarsen deliver benefits? It may be that lowering lp(a) in midlife after plaque accumulates is too late to confer reduction in MACEs—major adverse cardiovascular events. Administering it earlier—potentially after screening tests reveal high levels in childhood—could offer lifetime protection.
Alternatively, high lp(a) may be the smoke, not the actual fire; it may be merely a byproduct of a hitherto unknown risk factor that’s the correct target for suppression.
Hopefully, targeting lp(a) won’t prove to be another dead-end. Despite this initial failed clinical trial, the lp(a) story is most certainly not over as determined researchers recalibrate.
These and other stories like them are examples of my unique take on topics we cover on the Intelligent Medicine radio show, podcasts and here in our newsletter. Follow us at DrHoffman.com
