Findings may explain why the supposed link to food-borne saturated fats has faded
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Buildup of fatty plaque in the arteries is a defining factor in cardiovascular disease.
Arterial plaque consists of oxidized lipids (fats and cholesterol) plus pro-inflammatory immune chemicals and cells attracted to the site.
These deposits can narrow arteries, or break loose and clog them entirely, leading to heart attack or stroke.
Now, there's evidence that "alien" fats in arterial plaque — ones produced by common infectious bacteria — can trigger a damaging immune response that worsens the problem.
These new findings fit with the link between gum disease and artery trouble — and may help explain why recent research couldn’t link any specific dietary fat and plaque buildup.
(For more on new findings about dietary fat and plaque, see "No link found between arterial plaque and dietary fats", below.)
The potential implications of the new study become clearer when viewed against the historical background.
That fairly sad background features seemingly deliberate distortions with biases driven by sugar-industry funding.
The saturated fat theory of heart disease: A brief history
For decades, doctors and researchers assumed that the lipids that stuck to artery walls and formed plaque were regular saturated fats and/or cholesterol.
But we’ve always lacked solid evidence backing this hypothesis. In fact, people whose diets contain relatively large proportions of saturated fats — such as from eggs, butter, and red meats — don't always have higher rates of heart disease, with genetic and lifestyle factors playing key roles.
Blame fell on saturated fats even though the major early evidence featured data deliberately cherry-picked to produce the hugely influential “Seven Countries Study”, led by physiologist Ancel Keys, Ph.D.
Professor Keys first presented his hypothesis in 1956 — the same year that other scientists reported evidence linking heart disease to refined carbohydrates, especially sugar.
From the late 1950s through the early 1970s, Dr. Keys and his colleagues collected and analyzed diet and health data from 22 countries — but focused only on the seven countries where rates of heart disease were high, and people also ate relatively high proportions of saturated fat.
Subsequent analyses of the data collected from all 22 nations drastically undermined Keys' theory, and evidence that it was wrong has continued to accumulate.
Unfortunately, the misleading Seven Countries report led the U.S Congress and the American Heart Association to declare a public health war on saturated fat and cholesterol — one that has had little effect on rates of cardiovascular disease.
Growing doubts were fueled by a Harvard-led 2010 study that found “no significant evidence … that dietary saturated fat is associated with an increased risk of cardiovascular disease [CVD].” (Siri-Tarino PW et al. 2010)
And, as the same scientists wrote in a second study, “More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.”
They were referring to growing evidence that official urgings to replace saturated fats with polyunsaturated vegetable oils caused Americans to consume omega-6 fats in extreme excess.
Excessive intake of omega-6 fats yields the kind of chronic, “silent” inflammation that drives heart disease, dementia, and more.
And the average American's shortage of seafood-source omega-3s — which the body uses far more efficiently than plant-source omega-3s — exacerbates that problem: see Omega-3 Levels Beat Cholesterol at Predicting Death Risk.
To be sure, a small group of genetically unusual people need to limit intake of cholesterol and/or saturated fats, and take drugs as needed to manage heart risks.
But fast-growing evidence shows that for most people, the cholesterol and (most of the) saturated fats in foods are relatively harmless.
A recent review of the evidence from 15 clinical trials detected "a small but potentially important reduction in cardiovascular risk on reduction of saturated fat intake". (Hooper L et al. 2015)
However, the wording of that conclusion is contradicted by the scientists' specific finding that saturated fat intake had virtually no connection to the risk for stroke or for non-fatal heart attacks.
And its conclusions in favor of reducing intake of saturated fats — and replacing them with (mostly omega-6) polyunsaturated fats — are contradicted by those of several other evidence reviews.
For more on this topic, see Saturated Fat Seen as Heart Red Herring, Cholesterol Myth Busted for Good?, False Advice on Fats?, Big Sugar Paid Scientists to Pin Heart Disease on Saturated Fats, and Major Study Exonerates Saturated Fat, whose subtitle conveys its other key finding: “Big review sees no heart risk from saturated fat, but harm from omega-6-rich vegetable oils”.
New findings put bacteria-generated fats under the spotlight
University of Connecticut (UConn) researchers believe they may have solved part of the puzzle surrounding arterial plaque.
Their analysis of arterial atheromas collected from patients revealed lipids with a chemical signature unlike those produced by humans or other mammals (Nemati R et al. 2017).
Instead, these "alien" lipids come from a specific family of bacteria called Bacteroidetes, which produce distinctive fats.
The best-studied subgroups of Bacteroidetes bacteria include Porphyromonas, which are typically found in the human mouth, and — among other infectious oral bacteria — are clearly linked to cardiovascular disease.
When people have periodontal disease (of which they may be unaware), bacteria in the infected gum tissue can dissolve the barrier between the gums and the underlying connective tissue, causing inflammation.
And, when someone has periodontal disease, chewing or brushing can help bacteria enter the bloodstream, promoting inflammation and cardiovascular disease.
Indeed, oral bacteria that cause periodontal disease have frequently been found in the arterial plaque of people with gum and cardiovascular disease.
Bacteroidetes bacteria don’t usually infect the blood vessels, but the lipids they produce pass easily through cell walls and into the bloodstream.
The study’s coleader — Frank Nichols — is a UConn Health periodontist who studies the link between gum disease and atherosclerosis.
As he said about infectious oral bacteria, “I always call them greasy bugs because they make so much lipid [fat].”
Importantly, they make fats not typically produced by the bodies of humans or other mammals, so the immune system sees them as signs of infection.
Dr. Nichols' co-author, UConn chemist Xudong Yao, said the differences between bacterial and human lipids result in subtle weight differences between the molecules.
As he said, “We used these weight differences ... to selectively measure the quantity of the bacterial lipids in human samples ... a first step to mark the lipids as indicators for early disease diagnosis.”
The immune cells that migrate to blood vessel walls to consume unwanted lipids recognize Bacteroidetes lipids as foreign, leading them to attract more immune-system cells and trigger inflammation.
Nichols and Yao's team also showed that despite being non-native lipids, the Bacteroidetes lipids could be broken down by an enzyme in the body that processes lipids into the starting material to make inflammation-enhancing molecules.
Consequently, the lipids generated by Bacteroidetes threaten blood vessels in two ways:
- The immune system sees them as a sign of infection, fueling an immune response that promotes plaque buildup and arterial inflammation.
- Enzymes then break down these lipids, which super-charges the initial inflammation.
The next step for the UConn team is to analyze thin slices of atheroma to localize exactly where the bacterial lipids are accumulating.
If Bacteroidetes lipids accumulate mostly within arterial atheromas — rather than in healthy artery walls — that would provide strong evidence linking them to heart disease.
For sure, the UConn findings about inflaming bacteria lipids in artery plaque reinforces advice to brush and floss every day!
This research was supported by a grant from the National Institutes of Health.
No link found between arterial plaque and dietary fats
There’s ample evidence that lipid (fat and cholesterol) levels influence the risk of cardiovascular disease (CVD).
However, little has been known about their effect on the composition of arterial plaque, whose presence greatly raises the risk for heart attacks and strokes.
Recent studies have identified more than 150 genetic characteristics that influence blood lipid levels — providing a powerful tool for comparing blood lipids to the makeup of arterial plaque.
Three years ago, Dutch scientists reported what they found when they took advantage of the new tool to examine arterial plaque samples collected from 1,443 heart patients — people from whom samples of blood from their arterial plaque had also been collected.
The blood test data revealed the levels and proportions of four key determinants of cardiovascular health:
- HDL cholesterol
- LDL cholesterol
- Total cholesterol
Thanks to the genetic data collected from the patients, the Dutch scientists were able to calculate the “weighted genetic burden” scores (GBS) for genetic traits and all four of these major classes of lipids.
They then used statistical tools to compare the patients’ blood lipid levels and GB scores to seven features of the arterial plaque samples.
As expected, the patients’ GB scores reflected levels and proportions of lipids in their blood.
However, neither their blood lipid levels, nor their GB scores, could be linked to the microscopic features and characteristics of their arterial plaque samples.
In addition, neither the patients’ blood lipids nor their GB scores were linked to their cardiovascular health outcomes within three years of follow-up.
The only notable exception was that the composition of patients' HDL cholesterol did reflect lower risk for several adverse cardiovascular outcomes.
As the Dutch team wrote, “This study found no evidence that plasma lipid levels or their genetic determinants influence carotid plaque composition.”
Their findings suggest that the links between dietary fats and heart disease were never as simple as they were portrayed for decades.
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