I'm delighted to speak with you again and share my two-and-a-half-year experience involving several hundred patients utilizing 2-hydroxypropyl- -cyclodextrin, known as Cavadex, in the treatment of atherosclerotic vascular disease. Cavadex removes cholesterol from the vascular wall, cell membrane, lipid droplets, crystalline cholesterol, and oxysterols in a manner that generates nitric oxide, our natural vasodilator, while concomitantly reducing vascular inflammation. If you experience symptoms such as chest tightness or shortness of breath with effort due to a blocked coronary artery compromising blood flow to the heart muscle, or leg pain with walking due to lower extremity vascular disease (termed intermittent claudication), you are likely to experience initial symptomatic benefits within two to four weeks. During this timeframe, we are not rapidly opening your arteries this is a slow process that occurs molecule by molecule. Instead, we are improving blood flow through nitric oxide and anti-inflammatory effects.
With longer use three to six months and depending on your baseline symptomatic status, disease burden, and the identification and resolution of your risk factors (the underlying causes of your vascular disease), we anticipate that your symptoms will fully resolve with ongoing risk factor reduction and some form of maintenance therapy. This could involve Cavadex one to three times a week, one week a month, or over 30 days twice a year. With this approach, you should experience minimal symptoms and a low risk for future vascular events. Widespread acceptance and utilization of Cavadex could save millions of lives, spare the need for vascular procedures, and save billions of dollars in reduced healthcare costs and lost worker productivity.
Cavadex is not a drug; it is a naturally occurring molecule, a fermentation product of starch digestion. Drugs are man-made and not normally present in the human body. We use drugs to inhibit or block physiological processes that are pathologically overactive. When used expertly, drugs can help, and we use them frequently. However, drugs that inhibit biological processes can easily cause harm if overused. Cavadex does not block or inhibit bodily processes and cannot cause harm. Instead, it stimulates Mother Nature s reverse cholesterol transport program, working with our body to resorb plaque and restore normal blood flow. Cavadex in the U.S., and RemChol outside the U.S., is the trade name for 2-hydroxypropyl- -cyclodextrin, which we will refer to as cyclodextrin.
Cyclodextrin is used as a drug delivery vehicle and is a component of the Johnson & Johnson COVID-19 vaccine. The FDA lists cyclodextrin as GRAS (Generally Regarded as Safe) and has cleared it as an orphan drug for the treatment of Niemann-Pick disease, a pediatric cholesterol storage disorder. Thus, cyclodextrin is not new. What is new is that we are providing cyclodextrin to enable you to take charge of your vascular health. My name is James Roberts. I m board-certified and university-trained in internal medicine and invasive cardiology, a Fellow of the American College of Cardiology, and I ve completed coursework and passed written exams in chelation therapy, oxidative medicine, bariatric medicine, and anti-aging and regenerative medicine, where I m considered an advanced fellow. I teach the principles of integrative cardiology to physicians within integrative medicine training courses and have been involved in research on new drugs, devices, and nutraceuticals. With my colleague Dr. Rod Poling, we have initiated a 50-patient pilot study on the benefits of Cavadex in reversing coronary calcification.
Today, we will review the history of cyclodextrin and its development as a therapeutic agent, discuss Cavadex s mechanism of action, present case studies demonstrating its mechanisms and efficacy, and hear from several patients interviewed by Dr. [name omitted] who will share their stories in their own words. We ll also discuss how we use Cavadex in our practice, practical points, potential risks (which are minimal), and regulatory issues. I ll conclude with a summary.
Cyclodextrin is a fermentation product of starch. Dietary starch is a chain of glucose molecules bound together. Digestive enzymes break these bonds, converting starch to glucose, which we absorb and use to generate energy. In creating cyclodextrin, different enzymes break specific bonds within starch, forming ring structures called cyclodextrin. These are arranged as cone-shaped molecules, like a traffic cone, with alpha, beta, and gamma cyclodextrin variants. For human use, the most efficient is 2-hydroxypropyl- -cyclodextrin, which provides solubility in the circulation and avidly binds cholesterol from the vascular wall, removing it through the kidneys or to the liver. Cyclodextrin is used as a drug delivery vehicle. We administer unloaded cyclodextrin to pluck cholesterol out of the cell membrane. When mixed with a drug, it enhances solubility and uptake, and several prescription medicines contain cyclodextrin. The FDA considers it an inert excipient and has approved its use as a drug delivery vehicle.
The first human to receive intravenous cyclodextrin was in Australia in 1992, and researchers showed a significant amount of cholesterol in that patient s urine a profound finding that was not followed up at the time. However, animal studies demonstrated that cyclodextrin is safe, requiring ridiculously high doses (20 to 25 times greater than our rectal retention enema doses) to cause harm. The first human use of cyclodextrin was for Niemann-Pick disease, an autosomal recessive lipid storage disorder. If both parents carry one defective gene, a child with two defective genes cannot produce the Niemann-Pick protein that promotes cholesterol efflux from cells. These children can absorb and produce cholesterol but cannot eliminate it, leading to death before adolescence due to cholesterol overload, liver failure, and brain failure. Intravenous and subcutaneous cyclodextrin clears cholesterol from the liver but not the brain, as cyclodextrin does not cross the blood-brain barrier. To clear cholesterol from the brain, cyclodextrin is infused into the spinal canal, achieving high concentrations in the cerebrospinal fluid. This allows children to survive, though they may lose hearing due to excessive cholesterol removal from the brain a fair trade-off for survival.
Five to six years ago, Dr. Zimmer, a German researcher, published a paper showing that cyclodextrin reversed arterial disease in an animal model of human atherosclerosis. These animals lack LDL receptors and develop atherosclerosis, and every therapy effective in this model has translated to humans. This paper was brought to my attention by a physicist patient with premature atherosclerosis. I was intrigued but couldn t find a source of cyclodextrin and didn t pursue it further, assuming it was a drug or chemical we couldn t use. However, Kyle Hodgetts, a patient suffering from recurrent coronary disease and angina after multiple stents, read the same paper. To help himself, he obtained cyclodextrin and treated himself with intravenous doses, tracking his lipids and chemistries. He demonstrated that coronary disease could be reversed with cyclodextrin. Kyle s experience, shared on the Cholrem website, has helped humanity by highlighting Cavadex s benefits. In a few years, we may all be sipping champagne in Stockholm when Kyle receives the Nobel Prize for his contributions.
Let s discuss Cavadex s mechanism of action. Cavadex is a cone-shaped molecule with a water-soluble exterior, allowing it to exist in the circulation, and a fat-soluble inner cavity that can fit a cholesterol molecule. Envision your artery wall: its cells have semi-permeable, gelatinous membranes composed of cholesterol, triglycerides, and proteins, with molecules in constant Brownian motion. Occasionally, a cholesterol molecule pops out of the cell membrane. Being fat-soluble, it is attracted to the membrane and tends to return unless it encounters an HDL molecule, which can transport it to the liver and out through the stool. This is why high HDL levels are beneficial for removing cholesterol from the vascular wall. Cavadex is far more efficient than HDL at this task. When a cholesterol molecule leaves the cell membrane, it fits perfectly into Cavadex s cavity, which plucks it out. The cholesterol can then be excreted via urine or handed off to HDL, a low-affinity, high-capacity cholesterol carrier. Cavadex, with high affinity but low capacity (holding only one cholesterol molecule), transfers cholesterol to HDL, which grows larger and transports it to the liver. Cavadex then plucks another cholesterol molecule from the membrane.
As Cavadex removes cholesterol from the cell membrane, lipid droplets within the cell dissolve to replenish the membrane s cholesterol. Additionally, Cavadex removes diacylglycerols, a three-carbon backbone with two fatty acids that inhibit nitric oxide production, our natural vasodilator. Nitric oxide dilates arteries, provides a Teflon-like coating to prevent white cell and platelet adhesion, and is a vascular-protective chemical. Our modern diet, high in fats, reduces nitric oxide production. By removing cholesterol and diacylglycerols, Cavadex enhances nitric oxide production, explaining why patients feel better within weeks of starting therapy.
In patients with advanced, vulnerable plaques full of foam cells white cells engorged with oxidized lipids, mistaking them for microbes an immune response occurs, releasing inflammatory and oxidative mediators that drive atherosclerosis. These mediators convert smooth muscle and endothelial cells into foam cells, inflaming the entire artery wall. These inflamed cells rapidly incorporate Cavadex via pinocytosis, allowing it to access lipid droplets and crystalline cholesterol. Crystalline cholesterol is particularly malignant, promoting plaque destabilization and acute events. As Cavadex dissolves crystalline cholesterol, it creates oxysterols, prompting the body to generate cholesterol efflux pumps (e.g., ABCA1, ABCG1) that embed in the cell membrane and actively pump cholesterol out, docking with HDL. This transforms inflammatory foam cells into anti-inflammatory cells, reducing inflammation and oxidative stress, generating nitric oxide, and pumping cholesterol out of the artery wall. Everyone benefits from Cavadex, but the sicker you are, the greater the benefit, as foam cells avidly take up Cavadex, enhancing its anti-inflammatory and nitric oxide effects.
Does this translate to actual disease reversal? Yes. Kyle s angiogram showed plaque regression after Cavadex treatment. Of my approximately 200 patients treated with Cavadex, only two required repeat angiograms, suggesting the therapy s effectiveness, as repeat angiograms are typically needed only when patients are doing poorly. One patient, an 80-year-old man with severe three-vessel coronary disease, declined bypass surgery eight years ago, worked with an integrative physician, and started Cavadex nine months ago. After five months with me, addressing risk factors, he experienced chest pain on a cold day and was hospitalized. A repeat angiogram showed two vessels had closed, requiring bypass surgery. This could be seen as a failure of Cavadex, but I view it as too little, too late for a patient who could have had surgery years earlier.
Another patient, CJ, a 20-year patient of mine, had recurrent disease after a second bypass. Bypass grafts last about seven years on average, and he had done well with drug therapy, nutritional therapy, and enhanced external counterpulsation (EECP), a non-invasive method to augment collateral flow. A year and a half ago, chest pain prompted us to start Cavadex instead of EECP. He improved, but on a cold day, he had chest pain again. A repeat angiogram showed one vein graft had closed, but another, previously closed, had opened, and both received stents. He now takes Cavadex several days a week, has residual collateral-dependent disease, and is doing well.
We prefer non-invasive methods like CT angiograms. CC, a 62-year-old woman with chest tightness, hyperlipidemia, statin intolerance, and high lipoprotein(a), had a CT angiogram in April 2022 showing a 70% narrowing in her left anterior descending artery and a calcium score of 212 (90th percentile for her age). Her stress test was acceptable, so the narrowing was not critical, and stenting was not indicated. We started Cavadex and supportive therapies, and she improved. After four to five months, a repeat CT angiogram showed the narrowing reduced to mild-moderate (27% by AI analysis), with mild disease in the circumflex and right coronary arteries. She is now asymptomatic on weekly maintenance.
Coronary calcium scores reflect the extent and chronicity of atherosclerosis, progressing about 20% per year. Slowing progression to less than 15% annually is associated with favorable outcomes, while rapid progression predicts poor outcomes. No therapy has systematically reversed coronary calcification, but we are working on it. BP, a 59-year-old athletic man with hypertension, lipids, diabetes, high lipoprotein(a), and sleep apnea, had a calcium score of 37 in 2016 (79th percentile). By 2023, it rose to 265 (127% per year), prompting intensified therapy with vitamin K2 (to keep calcium out of arteries) and double-dose Cavadex for five months. His calcium score dropped 6%, demonstrating regression, and he remains asymptomatic, planning 30-day Cavadex courses twice a year.
RJ, a 75-year-old athletic man with atrial fibrillation, high lipoprotein(a), and chemical exposure, progressed 24% per year from 2015 to 2023. After five months of Cavadex, his calcium score regressed 8% (6% annualized), a significant finding. Kyle s experience and these cases suggest Cavadex may dissolve crystalline cholesterol, reducing calcification. Dr. Poling and I are conducting a 50-patient pilot study, enrolling patients with a full spectrum of arterial disease, treating them with 6 months of Cavadex (8g or 14g doses) alongside standard therapies. We anticipate systemic reversal of coronary calcification and will explore synergies with other drugs or supplements, hypothesizing that lower circulating cholesterol enhances Cavadex s efficacy by increasing the cholesterol gradient out of the arterial wall.
Carotid artery ultrasounds measure stenosis via velocity. SS, a 65-year-old man with high lipoprotein(a) and controlled hyperlipidemia, passed out from dehydration. An ultrasound showed a 90% blockage in his left internal carotid artery, refined to 65 70% by magnetic resonance angiogram not requiring surgery but needing monitoring. After four months of Cavadex and risk factor reduction, his carotid velocities fell, indicating artery opening. He plans four more months of Cavadex, expecting further improvement.
Cavadex enhances endothelial function, the artery wall s ability to generate nitric oxide, a key predictor of outcomes. We measure this non-invasively with a finger clip and blood pressure cuff to assess flow-mediated dilation. Patients show improved endothelial function with Cavadex, as it removes cholesterol and diacylglycerols, generating nitric oxide. Carotid intima-media thickness (IMT) ultrasound measures arterial wall thickness, reflecting plaque-forming propensity. A high IMT or rapid IMT progression predicts trouble. In high-risk patients post-open-heart surgery, rapid IMT progression correlated with events, while stable IMT predicted better outcomes. DB s IMT initially increased, then improved with Cavadex, suggesting a lag as the arterial ship turns around.
KH and SH, sophisticated patients with Lyme disease and cardiomyopathy, respectively, saw rapid IMT regression with Cavadex. SH s carotid bulb showed slight improvement after Cavadex, moving in the right direction. A 68-year-old woman with diabetes, high lipoprotein(a), statin intolerance, and a 70% LAD narrowing improved after two months of Cavadex, with a normal stress test and resolved symptoms after six months. Her IMT improved, and carotid ultrasound showed plaque regression, suggesting coronary plaque regression.
I tested Cavadex on myself. In 2008, my IMT was average for my age, with no plaque, but my left carotid IMT was worse, possibly from X-ray exposure during coronary angiograms. In 2022, I found mild plaque embarrassing for a marathon-running cardiologist. I received 50 IV Cavadex infusions (not optimally, at one to three times weekly) as a science project to ensure safety. My repeat IMT showed less plaque, with a transient increase then decrease, likely from arterial cells enlarging during cholesterol efflux. Cavadex lowered lipids in RS, a 69-year-old man with heart attacks and statin intolerance, whose cholesterol fell from 187 to 168 after three months. CI, a 50-year-old with three-vessel disease, avoided bypass surgery with Cavadex, reducing his LDL from 105 to 28 with pravastatin, herbal therapy, and Cavadex.
Cavadex may benefit heart failure patients. DA, a 79-year-old with atrial fibrillation, mitral regurgitation, kidney disease, and COPD, had a rising pro-BNP (a heart failure marker). After Cavadex, her pro-BNP fell significantly, and she felt better, likely due to nitric oxide s cardiac benefits. Side effects are minimal, primarily nuisance-related (e.g., gas, bloating from rectal administration). Hearing loss, seen in Niemann-Pick disease with spinal fluid infusion, does not occur with IV or rectal Cavadex, as it does not enter the brain. My hearing improved after 50 IV infusions, possibly from Cavadex or other therapies. Cavadex does not cause cholesterol deficiency, as it does not block cholesterol synthesis, only removing excess from the arterial wall.
In practice, we assess symptoms, disease burden (angiograms, calcium scores, ultrasounds), physiology (IMT, endothelial function), and risk factors, treating with Cavadex for three to six months. Symptomatic patients may use Cavadex twice daily initially, then once daily (8g, 10g, or 14g doses). Maintenance therapy (e.g., two to three times weekly or one month twice yearly) sustains remission. Regulatory issues arise as cyclodextrin is FDA-cleared as a drug delivery vehicle and GRAS, but some shipments from Australia were embargoed for labeling issues ( lowers cholesterol was deemed a drug claim). Relabeling as improves vascular health resolved this temporarily, but recent embargos cite Cavadex as an unapproved drug. I believe this is misguided, as Cavadex is a natural starch product, and FDA policy allows off-label use. We hope a new administration will embrace Cavadex, potentially covering it under Medicare, saving billions in healthcare costs.
In summary, Cavadex pulls cholesterol from the arterial wall, cell membrane, lipid droplets, crystalline cholesterol, and oxysterols, generating nitric oxide and reducing inflammation. Over time, it debulks plaque, as shown in carotid ultrasounds, CT angiograms, and calcium score reversals. Widespread adoption could save millions of lives, reduce vascular surgeries, and save billions in costs. My nearly four decades in cardiovascular medicine, now with Cavadex, allow me to help patients effectively, and I ll continue sharing updates on Cavadex and synergistic therapies.
Finally, I d like to highlight a cause close to my heart: the TBCK Foundation, supporting children with TBCK, an autosomal recessive condition like Niemann-Pick, where a protein deficiency disrupts cellular communication, leading to short lives and neural delays. Caring for these children is challenging, requiring feeding tubes and constant care. The foundation provides equipment (e.g., bathing apparatuses, stabilizing chairs) and funds research at Children s Hospital of Philadelphia into therapies like liposomes, mRNA, or viral gene delivery. Unlike pharmaceutical-driven research, TBCK research relies on private funding. Please visit the TBCK Foundation website, learn about this rare disease, and consider donating to support families and research. You can also purchase T-shirts, hoodies, or coffee mugs, with proceeds aiding families and research. Knowledge gained from TBCK may benefit other conditions. Thank you for your attention.
Hi, I'm Laurie Howes. I've been a professor of medicine for over 40 years, specializing in cardiology, particularly cardiovascular risk factor management and cardiovascular pharmacology. I have over 230 peer-reviewed manuscripts published in the area of clinical pharmacology, particularly cardiovascular pharmacology. I have a particular interest in the development of a compound called beta-hydroxy cyclodextrin. There are many cyclodextrins out there, so I think it’s important to know that this is one specific member of a large class that we’re studying because it has shown remarkable results in animal models of atheroma and some very interesting observational data from people who have received it for atheromatous disease.
Beta-hydroxy cyclodextrin is marketed in Australia and the USA under the trade name Cavadex. I use the word cyclodextrin, but you can easily substitute the word Cavadex, as most of the data has come from observations of people who have been placed on cyclodextrin therapy. It’s very important to emphasize that this specific kind has been shown to reverse atheroma and reduce plaque size in at least three animal models.
Over the last couple of years, I’ve been very proactive in trying to generate research into this remarkable compound and to increase our experience in the use of cyclodextrin to treat people with ischemic heart disease. There appear to be two major and separate effects of cyclodextrin in ischemic heart disease. The first is an immediate effect, which comes from the direct pharmacological effects of cyclodextrin, well-documented in animal studies and human studies using benchtop techniques. The second, and perhaps most important, feature of this compound is that it seems to be able to reduce the size of plaques, in other words, cause regression of atheromatous plaques in patients with ischemic heart disease. This provides an additional effect after the resolution of symptoms, which we can demonstrate quite well.
Cyclodextrin, therefore, has a dual function: one that is short-term, improving vascular inflammation and reducing the symptoms of angina, and another in the longer term, holding the promise of causing regression of plaque—something we’ve been unable to achieve with any other form of medical treatment thus far. The potential importance of cyclodextrin cannot be overstated. Cyclodextrin, in the form of Cavadex, has more safety data and more knowledge about its pharmacology than what we knew about statins when they were first introduced. I believe there’s potential for this treatment to be even more impactful than statins and certainly represents the greatest advance in cardiovascular pharmacology for the treatment of atherosclerosis since statins came on the scene.
The development of this treatment has largely been driven by one of my former patients, K. Hitt, who was not a fantastic role model in terms of how a person should look after their health and reduce the risk of heart disease. However, to his credit, he has made significant progress in getting people, particularly in the United States, to have experience with this compound, most of whom have had very substantial, demonstrated beneficial effects. At the moment, Cavadex has been given primarily to people with symptomatic heart disease for whom there is little else to offer in terms of revascularization. However, it has the potential to be used like statins, and probably in combination with statins, to cause regression of the disease and improve outcomes from a mechanical point of view.
This has enormous implications, not only for improving patients’ lives and symptoms but also for reducing demand on revascularization procedures, such as the implanting of stents, and perhaps even coronary artery disease itself. To put it into perspective, we have a potential treatment that may reverse coronary artery disease. Coronary artery disease is still the number one killer worldwide, and if we can make an impact using a medical treatment rather than surgical interventions, which have their own limitations, this would have a huge impact on public health.
I’ve been involved in cardiovascular research and the management of patients with ischemic heart disease for a long time. I have a substantial track record in research myself and was entered into Who’s Who in the World in 1998 for my contributions to medicine, as well as in a booklet called Marquis Great Minds of the 21st Century. There is still a lot we don’t know about cyclodextrin, and we hope to fill in the gaps in the future with more targeted, sophisticated research at both the laboratory and clinical levels.
It is very important that we press forward with gaining more experience in humans through clinical trial data. The unique situation with cyclodextrin is that it won’t generate significant profits for any particular person or company because it’s not readily patentable. It’s a compound we’ve been using to solubilize drugs in very high concentrations for over 30 years. Therefore, it’s critical that this unique opportunity does not slip away just because people can’t see a financial incentive. Cyclodextrin and the cyclodextrin family are essentially a form of starch, a natural byproduct of metabolism in humans. We’re talking about a natural compound with an enormous amount of safety data behind it. It’s very non-toxic and can be given in doses up to 20–30 grams a day, often used to solubilize drugs like antifungals. There’s no question about its safety, but we need further information on the extent of its benefits in humans because the promise it holds is truly unique.