Lowering Cholesterol with Whole Foods

A trusted food is one the label vouches for. A whole food is one the cell wall vouches for. Only the second is visible to your small intestine.

In the last issue I said I would swap wheat for barley, draw labs on 4 August, and publish the result including the one I did not want. The results are in. This time I got the one I wanted, and I also got three corrections to things I have said in print. Both belong here. I was so very happy to see the reversal of my ApoB trending downwards to my personal best. And I’m on a mission.

The larger question underneath the experiment is one of definition. I had been using the word whole to mean trusted. A trusted food is one that a brand, a health claim, a shelf position or a long personal habit has vouched for. Sprouted whole grain sourdough is trusted. Steel cut oats are trusted. Pearl barley is trusted. A whole food is narrower. It is a food whose plant cell walls are still closed when it reaches the duodenum, so the enzymes have to wait. Trust is a social fact. Structure is a physical fact. The artery responds only to the second.

The Result I Wanted

“Apolipoprotein B counts the number of atherogenic particles and is the better measure of risk when it and LDL cholesterol disagree.”

Sniderman, Thanassoulis, Glavinovic and colleagues. JAMA Cardiology, 2019.

June 30, 2026 my apolipoprotein B was 73 mg/dL. I reduced my wheat and bread consumption to once a week on July 21. On August 4, 2 weeks later, my apoB was 60 on Quest Labs and 59 on Access Labs. That is a fall of 13 points, about 18 percent, in 14 days, from one structural change to the carbohydrate.

Two weeks is fast, and it is fast for a reason that is well understood. LDL particles have a plasma residence time measured in days, so when hepatic receptor expression changes the circulating pool resets toward a new steady state within roughly 2 to 4 weeks. A 14 day draw catches most of the move but probably not all of it. If 14 days bought 13 points, the September draw 4 weeks later should tell me whether there is more underneath. The lipid panel from that Quest tube is still pending, so I do not yet have the LDL cholesterol, the triglycerides or the ion mobility particle count from that morning. Those 3 numbers are the ones that will confirm or complicate everything in this issue.

A Year of Yo-Yo’ing in the Neutral Zone Instead of the Reversal Zone

“The causal effect of LDL on the risk of atherosclerotic cardiovascular disease is determined by both the absolute magnitude of exposure and its cumulative duration over time.”

Ference, Ginsberg, Graham and colleagues. European Atherosclerosis Society Consensus Panel, European Heart Journal, 2017.
Table 1  Serial lipid markers
Table 2  Particle, inflammatory and metabolic markers

NMR is nuclear magnetic resonance and IM is ion mobility. Quest counted particles by NMR in June 2025 and January 2026 and by ion mobility in September 2025, November 2025, February 2026 and June 2026, so the particle columns cannot be read straight down as one series and each reference range is method specific.

Table 3 What coronary arrest and coronary reversal have required

These columns describe what the serial coronary imaging trials actually achieved in treated cohorts, not validated cut points for an individual. They come from the pooled intravascular ultrasound analysis in which substantial regression appeared in patients whose treated LDL fell below the trial mean of 87.5 mg/dL and whose HDL rose by more than 7.5 percent, from ASTEROID, where a mean LDL of 60.8 mg/dL produced a 6.8 percent median reduction in atheroma volume, and from the evolocumab imaging work showing regression continuing to very low LDL. The apolipoprotein B and blood pressure thresholds are inferred from their LDL equivalents and from guideline goals rather than measured as imaging endpoints, so read them as estimates. Higher HbA1c blunts plaque regression under otherwise adequate treatment.

The shape of 15 months is easy to describe and was uncomfortable to own. The first 12 weeks were a collapse in the right direction, from an LDL of 168 to 61 and an apolipoprotein B of 45. The following 12 months were a slow leak, due to my constant experimentations: Three walnuts. Three olives. A whole pomegranate on top of an already generous berry load. Bread I told myself was whole. By 30 June the apolipoprotein B had walked back to 73, which is roughly 60 percent more atherogenic particles arriving at the endothelium every hour than at my best. The August result does not undo that year. It shows the direction is still available.

Two rows deserve comment before the reader draws the wrong lesson from them. The hs CRP of 1.5 on 30 June is the only elevated inflammatory value in the series, due to me running a half marathon two days before the blood tests. I’m back down to 0.3 in August. A single high hs CRP is far more often a transient response to infection, travel or a hard training block than a change in baseline. 

The lipoprotein(a) row is more interesting. On the same Quest assay it has read 61, then 50, then 38 nanomoles per litre across 5 months. Lipoprotein(a) is largely genetically determined and is usually treated as fixed. A fall of that size is more than assay noise and I do not have a confident explanation for it. It is also worth noting that Access reported 24.1 mg/dL on the same day, but this mass result in milligrams cannot be converted cleanly into a molar result in nanomoles because the particle carries a variable number of repeat units. Whatever else is true, my lipoprotein(a) is not the dominant part of my risk, and it never was.

The Bread Was Never Removed

“Subjects who reported eating under 1,200 calories a day and could not lose weight were found to be underreporting their actual intake by 47 percent and overreporting their exercise by 51 percent, with no abnormality of metabolism.”

Lichtman, Pisarska, Berman and colleagues. New England Journal of Medicine, 1992.

I now log all my food for calories, macronutrients and micronutrients so I get an accurate archive. Here is a fact about the last 15 months that I have never put in writing, and it changes how the record should be read. From May 9, 2025 until July 21, 2026 I was eating bread every day. Typically 2 slices of ancient grain sourdough, more on training days, often with pasta alongside it. Every number in Tables 1 and 2 up to and including July 21 was produced by me eating flour daily inside a protocol that does not technically consider a true ‘whole food’.

That cuts both ways and I want both edges visible. The uncomfortable edge is that I spent 14 months describing myself as whole food plant based while eating a milled grain product every day, and I only noticed because I sat down in Kauai and audited myself honestly. The encouraging edge is more interesting. I reached an apolipoprotein B of 45 in August 2025 with the bread still in the diet. Bread was never the thing standing between me and my best number. It was one of several things sitting on top of it.

So the lever I pulled on July 21, was not the only lever, and the 13 points it bought in 14 days are not the ceiling of what removing it can do. Bread and pasta are now once a week, and typically before a 3 to 4 hour ride where the glycogen has somewhere to go and the working legs take the glucose up through a contraction driven pathway that does not need insulin at all. That is a budget, not a loophole, and I am going to keep saying so until I stop being tempted to treat it as one.

Two Laboratories for Truth

“When a new measurement method is compared with an established one, correlation between them is misleading. What matters is the size and the spread of the difference between paired readings.”

Bland and Altman. The Lancet, 1986.

I split the August 4 draw across both laboratories for one specific reason. My best apolipoprotein B, the 45 from August 2025, was an Access Labs result and every number since has been Quest, so I had no way of knowing whether I was comparing a real change or 2 different rulers. Quest read 60 and Access read 59. They agree to within a single milligram per decilitre. That settles it. There is no meaningful apolipoprotein B offset between these 2 laboratories, which means the 45 from last August was a true reading and not a laboratory artefact, and the drift up to 73 by June was equally real. I have a defensible baseline, a defensible best, and a defensible current number, all on the same scale. The particle counts are a separate question, because Quest counts by ion mobility and Access by nuclear magnetic resonance and the 2 methods do not return the same figure. The ion mobility count from that same tube is still pending, and until it arrives the rule is to compare each method only against itself and let apolipoprotein B referee.

What the Plaques Declare

“In patients with stable chest pain, low attenuation plaque burden on coronary computed tomography was the strongest predictor of fatal or non fatal myocardial infarction, ahead of calcium score, stenosis severity and conventional risk scores.”

Williams, Kwiecinski, Doris and colleagues. SCOT-HEART, Circulation, 2020.

The imaging can be stated in a paragraph. The coronary CT in June 2025 found 304.8 cubic millimetres of plaque across the whole tree. Of that, 199.7 is calcified and 104.7 is non calcified, so roughly 2/3 of my disease is scar and will not move and roughly 1/3 is live tissue that can. Low attenuation plaque, the lipid rich necrotic material that ruptures and kills people, measures 0.4 cubic millimetres in total, which is under a tenth of 1 percent of atheroma volume. In the first diagonal, the artery with the 77 percent narrowing, the movable fraction is 20.7 cubic millimetres and that is the specific target. On the carotid side, plaque that had been reported previously was gone by the August 2025 Carotid ultrasound, 3 months into the 10 percent fat whole food plant based diet, with no plaque visualised on either side. My disease is large, old and hard, and it is not unstable. Those are very different situations and the second is much the better one to be in at 55.

The Number I Want Is 45, then 38

“Among 198 consecutive patients with established cardiovascular disease counselled on a whole food plant based diet, adherent patients experienced a markedly lower rate of subsequent cardiac events than those who were not adherent.”

Esselstyn, Gendy, Doyle, Golubic and Roizen. Journal of Family Practice, 2014.

Dr. Joe Crowe was 44, a Cleveland Clinic surgeon, when he had a heart attack in November 1996 after a full day of operating. His distal left anterior descending artery was occluded in a position not amenable to a stent or a graft. He declined a statin, went on the 10% fat whole food plant based protocol, and brought his total cholesterol to 89 and his LDL cholesterol to 38. 32 months after the infarction the repeat angiogram showed the vessel filling again, 100%! Those 2 films sit side by side in Esselstyn's book, Prevent and Reverse Heart Disease, and they are, to me, the most consequential pair of images in cardiology.

I have been carrying that number, 38, for a year. It is worth being precise about why I am unlikely to repeat his result, because a target you cannot honestly reach is a target that will eventually make you dishonest.

Crowe reached a total cholesterol of 89 on food alone, which places him in genuine hyper responder territory. Most people, including me, likely do not have that liver. He was 44 with a fresh, soft, lipid rich lesion from an acute event. I am 55, with 304.8 cubic millimetres of plaque across all 3 territories, two thirds of it calcified, and a D1 that has been narrowing quietly for years rather than closing in an afternoon. At maximal adherence in 2025 I reached LDL 61, not 38.

So the goal has to be stated in the form the biology will actually accept. Calcified plaque is scar. It is stable, it is not going anywhere, and a calcium score that holds flat or rises modestly under good treatment is not a failure. Non calcified plaque is metabolically live tissue and it is the fraction the serial imaging literature repeatedly shows moving. My aim is to reverse as much of the 20.7 cubic millimetres of non calcified volume in the D1 as the biology allows, and to hold apolipoprotein B low enough and long enough that the remainder converts from live tissue into inert scar, as well as create ample collateral blood vessels and revive the endothelium of my arterial walls.

Which is why the number in front of 38 is 45. I have been there before, in August 2025, and I was there with bread still on the plate. Getting from 59 back to 45 is another 14 points, almost exactly the size of the drop I just made in 14 days, and this time the wheat is out as well. That is not a hope. It is a hypothesis with a test date on it.

If continued adherence lands me at 45 for apolipoprotein B and in the low 50s for LDL cholesterol this autumn, that is a real result and it is still short of Crowe. That is the point at which a powerful food or plant sterol or ezetimibe or bempedoic acid or a PCSK9 inhibitor question stops being theoretical and becomes a decision to make with my cardiologist rather than one to defer. An apolipoprotein B of 59 says the food is working. It does not yet say the food is enough.

My Top 5 LDL Lowering Foods

“In 46 hyperlipidemic adults, a portfolio of cholesterol lowering foods (portfolio diet) reduced LDL cholesterol by 28.6% in 1 month, against 30.9% for 20 mg of lovastatin and 8 percent for a conventional low saturated fat diet.

Jenkins, Kendall, Marchie and colleagues. JAMA, 2003.

Every food I am about to list is worth single digits. The CUT or subtraction is worth 10 times more than any of them, and if the order of operations is wrong then nothing else matters. Cut 1st. Add 2nd.

The size of the cut is not a guess. In Esselstyn original series, 18 severely ill patients who adhered to the diet brought a mean total cholesterol of 237 mg/dL down to 137 at 5 years, a fall of 42%, and 11 of them who had repeat angiography showed no additional stenosis with 8 showing regression. In his 2014 follow up of 198 consecutive patients with established cardiovascular disease, 177 were adherent, and across a mean of 3.7 years there was 1 stroke among those 177 against 13 major events among the 21 who were not adherent. My own cut took LDL cholesterol from 167 to 61 in 12 weeks, a fall of 63%. Removing oil, dairy, meat and refined flour is worth somewhere between 30% and 50%. Nothing you add to a plate approaches that.

What follows is the second lever, and the honest way to read the table is that these effects ADDing a stack and the ceiling of the whole stack is around 25% to 30%. The barley and oats act by beta glucan via bile acids, similar to psyllium husk, which I tried but didn’t add enough incremental decrease for me so I stopped it. Grapefruit via the liver. Lentils and beans another mechanism. I plan to do a separate newsletter to do a deep dive on the mechanisms of this so that your strategy of food choices becomes clearer in the future.

Table 4  My top LDL lowering foods

A 5% reduction on an LDL of 160 is 8 mg/dL. The same 5% on an LDL of 80 is 4. The lower you already are, the less absolute movement each addition buys, which is the arithmetic reason the cut has to come first.

The grapefruit needs a warning attached to it every single time it is mentioned, and I am not going to bury it in a footnote. Grapefruit contains furanocoumarins that irreversibly inhibit the CYP3A4 enzyme in the intestinal wall, which is the enzyme that breaks down a long list of common drugs before they reach the bloodstream. Block it and the drug is absorbed at several times the intended dose. The list includes simvastatin, lovastatin and atorvastatin, where the consequence can be muscle breakdown and kidney injury, along with amiodarone, several calcium channel blockers, tacrolimus, cyclosporine and some benzodiazepines. The inhibition is irreversible and lasts until the gut makes new enzyme, which takes about 24 hours, so you cannot time your doses around it and juice is no safer than the fruit. If you are on any of these, do not add grapefruit without asking your physician first. Pravastatin, rosuvastatin and pitavastatin are generally not affected, and a PCSK9 inhibitor is an injected antibody that has nothing to do with this pathway at all.

That leaves the question of how far food can actually go, and there is one trial that answers it more cleanly than any other. Jenkins and colleagues took 46 healthy but hyperlipidemic adults, 25 men and 21 postmenopausal women, mean age 59 with a mean body mass index of 27.6, and randomised them for 1 month to 3 arms. A conventional very low saturated fat diet dropped LDL cholesterol by 8 percent. Twenty milligrams of lovastatin dropped it by 30.9 percent. A diet built from viscous fibre, plant sterols, soy protein and almonds dropped it by 28.6 percent, statistically indistinguishable from the drug.

The counterweight belongs in the same paragraph. That trial was metabolically controlled and the food was provided. When the same group ran the portfolio under real world conditions where participants shopped and cooked for themselves, only about a third of motivated people achieved a reduction greater than 20 percent. The ceiling of food is roughly a statin. 

So my strategy for the next 12 weeks is stated in order rather than as a list. The cut is already made and it is the thing I protect. Then barley and oat groats every day for the 3 grams of beta glucan, lentils or black beans every day for the pulse effect and the resistant starch that comes with them, a red grapefruit daily because I am on no interacting medication and 20 percent in 30 days in bypass patients is the largest single food effect in the table, and spirulina retained on the understanding that its true effect is variable. Getting apolipoprotein B from 59 to 45 is a 24 percent move, which is a portfolio sized ask being made from an already low starting point. That is the honest measure of how hard this next stretch is, and it is why the answer in September will be interesting whichever way it falls.

The Grain I Cannot Find

“Across pearling fractions of 15 barley cultivars, protein, ash and antioxidant activity fell from the outer layers to the inner ones while beta glucan showed the opposite trend.”

Irakli, Lazaridou, Mylonas and Biliaderis. Foods, 2020.

Bread and pizza, both of which I love, are now a once a week event rather than a daily one, and when I do eat them it is an ancient grain sourdough, einkorn, emmer or kamut. In their place I have put barley, for the beta glucan, and oat groats in place of steel cut oats.

This is where the trusted food problem announced itself. I went looking for hulled barley, the true whole grain in which only the inedible outer hull has been removed and the bran is fully intact, and I cannot reliably buy it. What is on every shelf is pearl barley, abraded to strip the hull and part or all of the bran. It is the same relationship as steel cut oats to rolled oats, or more exactly the relationship between oat groats and steel cut oats, which is why I moved to groats. The groat is not cut at all. I cook it like rice and it is genuinely delicious, chewier and nuttier than anything a steel cut oat produces.

Now the part that surprised me and that changes the practical answer. In wheat the fibre is concentrated almost entirely in the bran, so milling it away is catastrophic. In barley the beta glucan is distributed throughout the endosperm and actually increases toward the inner layers of the kernel. The pearling studies show protein, ash, phenolics and antioxidant activity falling as you move inward while beta glucan rises. Pearl barley therefore loses the bran fibre, the minerals, the ferulic acid and most of the antioxidant capacity, and yet retains a great deal of its beta glucan. It is a compromise. It is not the disaster that white flour is.

What pearling does destroy is structure, and structure is the whole argument of this issue. The intact cell walls that force the enzymes to wait are abraded away, so pearl barley digests faster than hulled. My working answer is practical rather than pure. I will use pearl barley when it is what I can buy, and I will restore what pearling took by cooking and cooling it. Cook a large batch, refrigerate overnight, reheat portions through the week. The amylose retrogrades into resistant starch type 3 and the melting temperature of that crystal is high enough that ordinary reheating does not undo it.

Three shelf terms are worth knowing before the next grocery trip. Pot barley, sometimes sold as Scotch barley, is lightly pearled and sits between hulled and pearl. Hulless or naked barley is a cultivar whose hull threshes free in the field, so it needs no pearling at all and is a true whole grain by default. It is the one worth ordering by mail if the local shelves will not cooperate. And the word intact on a package means more than the word whole.

Table 5  Trusted foods and their whole food equivalents

The test in the third column is always the same. Ask whether the plant cell wall is still closed when the food reaches the small intestine. If the answer is no, the food is processed regardless of what is written on the bag.

I have to be honest about the weekly sourdough, because I am the one who will be tempted to launder it. Einkorn and kamut are older wheats with different gluten and, in a long fermentation, a somewhat lower glycemic response. None of that restores a cell wall that a roller mill has already destroyed. The weekly loaf is a budgeted pleasure inside a protocol that formally excludes it. That is a defensible thing for a 55 year old man to choose. It is not a whole food, and I am done calling it one.

Subtracting the Shelf

“In a double blind randomised study, 1 gram of daily vitamin C reduced the training induced improvement in maximal oxygen uptake and blunted the expression of the transcription factors that drive mitochondrial biogenesis.”

Gomez-Cabrera, Domenech, Romagnoli and colleagues. American Journal of Clinical Nutrition, 2008.

The same reasoning that took the bread off my plate took roughly 80 percent of the bottles off my shelf. A supplement is the most processed food object in the house. It is a single molecule, isolated from the matrix that carried it, at a dose no plant has ever produced. If structure is the active ingredient, I cannot keep a shelf of isolated molecules and call myself consistent. What remains is spirulina. Next month I will add 500 mg of vitamin C, on hard rides only, at a deliberately small dose because the exercise induced oxidative stress I would be buffering is also the signal I am training to produce. Otherwise the ascorbate arrives inside an orange or a papaya.

On the long rides I eat dried figs and dates, and that does not contradict the pomegranate correction from January. Fructose eaten at rest bypasses phosphofructokinase, the main regulated checkpoint of glycolysis, and flows toward lipogenic substrate without feedback control. During exercise, muscle contraction recruits glucose transporters to the cell surface independently of insulin and the working legs are an enormous sink competing for that substrate before the liver ever sees it. Sugar during a 4 hour climb is fuel. The same sugar on the sofa is a lipogenic signal.

The riding is deliberately structured. I hold an average heart rate around 140 to 150 with a ceiling of 170. Against a measured maximum of 195 that is 72 to 77 percent of maximum for the bulk of the work, with the ceiling at 87 percent.

Trusted, Not Whole

“Intact plant cell walls physically encapsulate the starch and fat held inside them and limit the access of digestive enzymes, so the same nutrients in a milled food and an intact one are not equally available to the body.”

Grundy, Edwards, Mackie, Gidley, Butterworth and Ellis. British Journal of Nutrition, 2016.

The simple believes everything, but the prudent gives thought to his steps. Proverbs 14:15. I have read that verse for years as being about gullibility toward people. It is at least as much about gullibility toward objects, and toward your own earlier sentences. The simple man is not reckless. He is untested in his trust.

I trusted the bread because it was sourdough and half whole grain. I trusted the oats because they were steel cut. I trusted a carotid comparison because the numbers moved in the direction I wanted.

So the record now reads as follows. Apolipoprotein B 73 to 59 in 14 days on one structural change to the carbohydrate, after 14 months in which I ate bread daily and called it whole. Two thirds of my plaque is calcified and will not move. The third that can move is about 105 cubic millimetres, of which 20.7 sits in the artery I care about most, and almost none of it is the low density material that kills people. Inflammation is quiet and glucose handling is clean. The mechanism I have been writing about for a year is now visible in my own blood, which is the least common outcome in self experimentation and the only one worth waiting for. The next labs are in early to mid September at 4 to 6 weeks, then week 8, then week 12, and I will publish all of them, including the ones I do not want.

A Request

Each Saturday I upload a new video to my Youtube Channel. Please like, comment and subscribe so that this reaches the people in your network who need it. It is my mission to help people avoid the heart attack, the stroke and the sudden death that I very nearly succumbed to myself.

Your Question

A question worth exercising with

For yourself. For someone you love. Answer this question in the quietness of your day.

Which food in your kitchen do you trust most and which do you now trust least, and when did you last look at what it is actually made of?

  • Consider removing the one that is not beneficial to you or even, harmful to you starting today for the next 3 months.

For Someone You Love

There is someone in your life eating carefully and still moving in the wrong direction. You thought of them. Send this to them. Your loved ones just need the information to act and a guide to help them.

Keep going. The race is long, the road is beautiful, and the body was built to heal. Grace, strength and love to you.

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Kevin Ham, MD