A medical explanation of how food-as-medicine could work
The food-as-medicine movement is gathering steam, bringing hope that growers producing healthier food will be rewarded with higher prices. Yet it remains a movement that needs more supporting data. There is not much scientific evidence that “health food” is, in fact, healthier for people or animals. For example, it seems intuitive that removing pesticides from food must make it healthier, but no studies have demonstrated a clear benefit — there is, as of yet, no evidence that food grown this way adds to lifespan or improves any measure of health.
Still, new evidence is emerging, and those active in this field will be more effective if they have some knowledge of the medical side of the equation. This article focuses on atherosclerotic cardiovascular disease (ASCVD) and how food can influence the disease process. Why ASCVD? Because it is the most common cause of death, because it turns out to be an inflammatory condition, and because, as a cardiologist, I understand it (an oncology researcher could tell a similar story about cancer!).
Heart Attack and Inflammation
ASCVD is caused by “cholesterol plaque” that blocks arteries supplying the heart (leading to heart attacks) or the brain (causing strokes). Arterial plaque develops over a lifetime; autopsy studies of young soldiers killed in three wars found developing plaque in more than half.
The first step in plaque formation is oxidation of low-density lipoprotein cholesterol (LDL), the infamous “bad cholesterol.” Oxidized LDL penetrates the artery wall and triggers a cascade of inflammatory reactions with white blood cells (lymphocytes), interacting with other arterial wall cells. The outcome is an atherosclerotic lump that partially blocks the artery. A plaque is composed of a lipid/cholesterol core, separated from the bloodstream by a fibrous cap (see Figure 1). If the cap erodes or ruptures and lipid contents are exposed to blood, a blood clot (thrombus) forms, potentially blocking the artery completely. In the 1950s, heart attacks were called coronary thrombosis for just this reason.
Oxidation and inflammation fuel this process in two ways: (1) the slow, decades-long buildup of plaque (chronic ASCVD), and (2) the acute event, in which the plaque’s surface is disrupted, causing thrombosis and a heart attack.
Chronic ASCVD: If it starts with oxidation of LDL, what causes that oxidation? Evidence suggests that inflammation elsewhere in the body, “systemic” inflammation, is involved. Population studies have linked intense inflammatory illnesses early in life to a higher risk of heart attack decades later.
Consider the heart attack epidemic in mid-20th-century America, when rates doubled (see Figure 2). Diet changes and increased cigarette availability did not account for this rise, and we had no explanation for why it went away by the end of the century. Indeed, death from heart attack is back at the baseline rate despite the obesity epidemic.
The likely culprit was the Spanish flu of 1918 that killed 50 million worldwide (compared to 7 million from COVID-19). For unknown reasons, young adults were targeted by that year’s influenza virus, which triggered overwhelming inflammation. It happened fast; a 20-year-old developed cough and fever, then influenza pneumonia, and died with lung congestion in three days. Survivors were left with a hidden legacy: oxidized LDL and plaque-promoting lymphocytes. ASCVD developed, and when this generation reached their 50s to 70s, heart attack rates spiked. As that generation passed away toward the end of the century, the heart attack epidemic receded.
There was a similar earlier occurrence — probably from a measles epidemic in late-18th-century France. The affected generation had shorter stature (documented when drafted by Napoleon in the 1790s), and an increased cardiac death rate at age 70. We may see a post-COVID uptick in heart attacks 40-50 years from now.
Acute heart attack: Systemic inflammation also boosts near-term heart attack risk. Generalized inflammation triggers plaque inflammation. Bacterial pneumonia increases heart attack risk over the following months eightfold, influenza and COVID quadruple it, and urinary tract infections triple it. The effect parallels the level of inflammation. Chronic non-infectious inflammatory illnesses — rheumatoid arthritis, lupus, asthma and abdominal obesity (since belly fat produces inflammatory cytokines) — also increase risk.
Preventing or reducing inflammation lowers this risk. For example, people vaccinated against flu and COVID-19 don’t have more near-term heart attacks; vaccination reduces the chance of infection by 70 percent, and the 30 percent who do get it have milder illness. Likewise, asthma raises heart attack risk, but not for those using steroid inhalers.
Those with unstable ASCVD always have elevated CRP, a key inflammation biomarker. The inflammatory white cells in the lipid core produce enzymes that can weaken the fibrous cap, making it prone to rupture (Figure 1, middle). Furthermore, the process is not localized to the plaque that causes the heart attack. Arterial plaque elsewhere in the body has the same unstable composition; it is a system-wide process.
To sum up: systemic inflammation and oxidation provoke heart attack in two ways. First, early-life inflammation fosters LDL oxidation, starting a lifelong buildup of arterial plaque. Second, acute inflammation later in life can trigger the final event — plaque inflammation, rupture, thrombosis and heart attack. Oxidation and inflammation also play key roles in many other chronic diseases.
Limiting Inflammation via Food
Food can be medicinal if it blocks oxidation and inflammation. Plants offer this with phytochemicals — polyphenols, phytosterols and carotenoids that are responsible for color, aroma and flavor. New data relate farming practices that boost phytochemical levels to measurable health benefits.
In a 2022 article published in PeerJ (doi.org/10.7717/peerj.12848), Montgomery, Bikle, Archulueta, Brown and Jordan compared corn, soybeans, peas and sorghum from 20 U.S. farms. Ten of them had used regen ag methods for more than three years, and the other ten were conventionally farmed controls. The regenerative farms produced crops with not only increased nutrient density but also higher phytochemical content. A health benefit emerged in livestock in their study (although they did not emphasize it in their report); beef and pork from regeneratively raised animals had a healthier fatty acid profile — a measurable health outcome. They attributed this benefit to a phytochemical boost in forage created by increased soil microbial mass and diversity.
A similar result has been reported from the use of live, mixotrophic Chlorella vulgaris as a biostimulant. In spring 2025, Bryan Mussard of Reminisce Angus Ranch in Montana observed that 125 heifers grazed for three months on 80 acres treated with Chlorella vulgaris were heavier, their artificial insemination failure rate was 5 percent instead of the usual 15 percent, and their mineral supplement consumption fell by 90 percent. For another group of two-year-old cows, results were similar. Reminisce Ranch had not been managed with regen ag practices, but the pasture and hay fields have been no-till. For four years, he had used a single annual Chlorella vulgaris application on native grass and two on hay. Increased microbial biomass and diversity are consistently described by growers who soil test when using Chlorella vulgaris. Dr. Montgomery is probably right when citing microbial biodiversity as the source of phytochemical generation.
The lesson of this story is not that algae itself makes cattle healthier. It was the food grown with algae, or with regen ag, that made the animals healthier: food as medicine, not algae as medicine.
Background Anti-oxidation
These biological systems are complicated; many thousands of phytochemicals have been identified. Throughout history, humans have extracted medicines from plants (like salicylic acid and aspirin). Plant-based medicines are not nutrients but organic compounds like polyphenols. We concentrate them in pills for short-term, high-dose therapy.
But how can eating plants with tiny amounts of these compounds be medicinal? The answer may be volume and time: a person consumes them in small quantities with food, every day over a lifetime, providing a consistent, low-level background of antioxidants. If a plant has more of these phytochemicals, it is “more medicinal.” A continuous low dose of these plant compounds may work better than sporadic, high-dose supplementation (which is never lifelong).
In short, we have early evidence that foods grown with regenerative agriculture, or with a live-cell algae biostimulant, may be healthier because of increased phytochemical content. Current data are observational, and further research is needed to confirm benefits and understand mechanisms, but consider these possibilities:
- Phytochemical and antioxidant capacity are measurable, allowing for standardized “healthiness” metrics. Food packaging may soon display the phytochemical content or a polyphenol/antioxidant index.
- Consumers will learn about these benefits through grocers eager to market them.
- Multiple ranchers note that cattle prefer algae-grown grass and hay; it tastes better, and that is related to phytochemical content. Strawberries and citrus grown with algae have a more vivid taste — they aren’t just sweeter.
- Large buyers — grocers, potato chip makers, those in the fast-food industry — can influence their suppliers’ farming practices. They could champion food-as-medicine approaches as a public service. They may also consider funding developmental research, beginning with well-designed animal trials.
- Consumers will pay more for verifiably healthier food. There are few regen ag growers in the U.S. Demand for this food will exceed supply.
Dr. Taylor finished his career at the Medical University of South Carolina as a cardiologist and clinical researcher. He is now the founder and chief science officer of The Live Cell Algae Group.
