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First-in-Class Drug Targeting Treatment-Resistant High Blood Pressure Wins FDA Approval — and Works Like No Existing Drug
High blood pressure — hypertension — is the single most treatable risk factor for cardiovascular disease and stroke, the two leading causes of death in the United States. There are already more than a dozen classes of antihypertensive medications. For most patients, combining two or three of these drugs in appropriate doses achieves adequate blood pressure control and dramatically reduces the risk of heart attack, stroke, kidney failure, and premature death.

But for a significant subset — estimated at 10 to 15 percent of all hypertensive patients — blood pressure remains uncontrolled despite taking two, three, or even four medications at maximum tolerated doses. This is called resistant hypertension, and it represents one of the most clinically frustrating situations in internal medicine: a patient taking a handful of pills every day, experiencing their side effects, and still not achieving the blood pressure target that determines their future risk of cardiovascular catastrophe.

For these patients, the FDA’s May 18, 2026 approval of baxdrostat (Baxfendy) — developed by AstraZeneca — represents the arrival of a fundamentally new therapeutic option built on a mechanism of action that no previously approved drug has ever targeted in this indication.

“We have been waiting for an innovative medication like BAXFENDY for hypertension for many years,” said Bryan Williams, MD, Chair of Medicine at University College London and a primary investigator for the pivotal BaxHTN trial. “Its novel way of lowering blood pressure has the potential to transform clinical practice by targeting a root cause of persistently uncontrolled hypertension.”

The Aldosterone Problem and Why Existing Drugs Miss It

Aldosterone is a steroid hormone produced by the adrenal glands that regulates sodium and water retention in the kidneys. When aldosterone levels are excessive — whether due to a benign adrenal tumor (primary aldosteronism), stress-related overproduction, or other dysregulation — the kidneys retain too much sodium and water, blood volume rises, and blood pressure increases in a way that does not respond well to most standard antihypertensive mechanisms.

The renin-angiotensin-aldosterone system (RAAS) is already a major target of existing hypertension drugs: ACE inhibitors, ARBs, and direct renin inhibitors all interfere with the pathway that leads to aldosterone production. But these drugs do not directly target aldosterone synthase — the specific enzyme, encoded by the CYP11B2 gene, that is the final step in aldosterone manufacturing in the adrenal gland. Blocking earlier steps in the RAAS leaves aldosterone synthase activity largely intact, allowing it to produce aldosterone through compensatory mechanisms.

Baxdrostat is a selective aldosterone synthase inhibitor — a small-molecule oral drug that directly and selectively inhibits CYP11B2, preventing aldosterone from being synthesized in the first place. This selectivity is critical: the enzyme CYP11B1, which produces cortisol and sits in a closely adjacent biochemical pathway, is not significantly affected by baxdrostat at therapeutic doses. This means baxdrostat lowers aldosterone — and therefore blood pressure — without disrupting the cortisol axis that regulates the stress response, immune function, and metabolism. AstraZeneca confirmed in clinical trials that baxdrostat lowered aldosterone levels without affecting cortisol levels.

What the BaxHTN Phase 3 Trial Found

The BaxHTN trial enrolled 796 patients with uncontrolled or resistant hypertension — all already on at least two antihypertensive agents, including a diuretic — and randomized them 1:1:1 to receive baxdrostat 2 mg once daily, baxdrostat 1 mg once daily, or placebo in addition to their background therapy, for 12 weeks.

At week 12:
- Patients on baxdrostat 2 mg had a 15.7 mmHg reduction in seated systolic blood pressure from baseline — a 9.8 mmHg placebo-adjusted reduction.
- Patients on baxdrostat 1 mg had a 14.5 mmHg reduction — an 8.7 mmHg placebo-adjusted reduction.
- The placebo group had a 5.8 mmHg reduction from baseline.
Both doses met the primary endpoint of statistically significant systolic blood pressure reduction. The findings were consistent in patients with both uncontrolled hypertension (not at goal despite two or more drugs) and truly resistant hypertension (not at goal despite three or more drugs, including a diuretic). Results were also supported by a separate Phase 3 Lancet-published Bax24 trial using ambulatory blood pressure monitoring, confirming the effect on 24-hour blood pressure rather than only the clinic reading.

A 9.8 mmHg reduction in systolic blood pressure is not a cosmetic number. Systematic reviews of blood pressure interventions consistently show that each 5 mmHg reduction in systolic blood pressure reduces the risk of major cardiovascular events by approximately 10 percent. For patients whose blood pressure has been inadequately controlled despite multiple medications — meaning they have been living with elevated cardiovascular risk despite treatment — a nearly 10 mmHg additional reduction is clinically meaningful and potentially life-extending.

Who Will Benefit and What Comes Next

Baxfendy is approved as an add-on oral treatment for adults with hypertension not adequately controlled on other medications. It is taken once daily in 1 mg or 2 mg doses. The key safety considerations identified in trials are hyperkalemia (elevated blood potassium), which requires periodic monitoring, and hyponatremia (low sodium) in some patients. Neither was dose-limiting in the vast majority of trial participants.

The drug received Fast Track and Breakthrough Therapy designations from the FDA during development, signaling the agency’s recognition of the unmet need it addresses. AstraZeneca is also studying baxdrostat in additional conditions where aldosterone excess plays a mechanistic role, including chronic kidney disease and heart failure — conditions that frequently co-occur with resistant hypertension.

Frequently Asked Questions

Q: What is baxdrostat (Baxfendy) and who is it for?

A: Baxdrostat is the first-ever oral aldosterone synthase inhibitor, FDA-approved May 18, 2026 as an add-on treatment for adults with hypertension not adequately controlled on other antihypertensive medications.

Q: How does baxdrostat work differently from other blood pressure drugs?

A: It directly and selectively inhibits aldosterone synthase (the CYP11B2 enzyme), preventing aldosterone production at its source. No previously approved drug has targeted this specific enzyme. Existing RAAS drugs act earlier in the pathway and leave aldosterone synthase partially active.

Q: How much does baxdrostat lower blood pressure?

A: In the BaxHTN Phase 3 trial, baxdrostat 2 mg added to background therapy produced a 9.8 mmHg placebo-adjusted reduction in systolic blood pressure at 12 weeks. The 1 mg dose achieved an 8.7 mmHg reduction.

Q: Does baxdrostat affect cortisol levels?

A: No. Baxdrostat selectively inhibits CYP11B2 (aldosterone synthase) without significantly affecting CYP11B1 (cortisol synthesis). Clinical trials confirmed aldosterone reductions without changes in cortisol.

Q: What are the main side effects of baxdrostat?

A: Hyperkalemia (elevated potassium) and hyponatremia (low sodium) are the primary safety considerations, both requiring periodic monitoring. Neither was dose-limiting in most trial participants.
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June 14, 2026
CRISPR Gene Editing Achieves a Functional Cure for Sickle Cell Disease in 96 Percent of Patients — RUBY Trial Results in the New England Journal of Medicine Are Historic

The phrase “functional cure” is used carefully in medicine — it describes an outcome in which a disease’s effects are so effectively suppressed that the patient lives as though they do not have it, even if the underlying genetic cause remains. For sickle cell disease, a condition that has caused lifelong suffering, organ damage, and premature death for 100,000 Americans and millions globally, achieving a functional cure through gene editing is one of the most profound accomplishments medicine has produced in years.

The RUBY Trial, published in the New England Journal of Medicine on April 1, 2026, has delivered exactly that result. Of 28 patients with severe sickle cell disease who were treated with renizgamglogene autogedtemcel (reni-cel) — a CRISPR-Cas12a gene editing therapy that modifies patients’ own blood-forming stem cells — 27 (96 percent) had no painful sickle cell crises for up to two years following treatment. Their average hemoglobin levels rose to near-normal levels, effectively restoring the oxygen-carrying capacity that sickle-shaped red blood cells cannot provide.

“We have seen that a benefit of this CRISPR/Cas12a gene-editing technology is that there is no rejection, so it’s different from traditional bone marrow transplants, which is standard treatment for sickle cell patients currently,” said Dr. Rabi Hanna, lead author and chair of the Pediatric Hematology-Oncology and Blood and Bone Marrow Transplant Division at Cleveland Clinic Children’s, who led the multicenter trial sponsored by Editas Medicine. “Our aim has been to achieve a functional cure to help prevent any future damage caused by sickle cell disease, and these latest results are compelling.”

How Reni-Cel Works — and Why Cas12a Matters

Reni-cel uses CRISPR-Cas12a gene editing to target the promoter regions of the HBG1 and HBG2 genes — the switches that normally suppress fetal hemoglobin production after birth. By editing these promoters, reni-cel reactivates the production of fetal hemoglobin (HbF) in adult red blood cells. Since fetal hemoglobin does not sickle, its presence in sufficient quantities effectively dilutes or displaces the dysfunctional sickle hemoglobin, preventing the cell deformation that causes sickle cell crises, organ damage, and shortened life expectancy.

This approach is distinct from Casgevy (exa-cel) — the first approved CRISPR therapy for sickle cell disease, using CRISPR-Cas9 to target BCL11A, a different suppressor of fetal hemoglobin. Reni-cel uses CRISPR-Cas12a, which has a different molecular structure and cutting mechanism from Cas9, and targets HBG1/HBG2 directly rather than through BCL11A. The two approaches achieve similar biological endpoints — fetal hemoglobin reactivation — through different molecular pathways, meaning they may offer complementary options for patients in whom one approach is less effective.

The 28 patients — four of whom were treated at Cleveland Clinic Children’s — underwent a procedure in which their stem cells were first collected and taken to a laboratory where the gene editing was performed. They then received chemotherapy to clear their bone marrow, making room for the repaired cells, which were infused back into their bodies. Within weeks of engraftment, fetal hemoglobin levels began rising. Most patients’ hemoglobin reached near-normal values within the first several months — and the patients themselves experienced what the data describe: two years without a painful crisis.

Access and What Comes Next

Reni-cel is not yet FDA-approved. The RUBY Trial data represent Phase 1/2 trial results — sufficient to demonstrate safety and early efficacy, but additional confirmatory data and FDA submission will be needed before approval. Editas Medicine, the trial sponsor, is expected to proceed with regulatory submission based on these results. The cost challenge that affects Casgevy — approximately $2.2 million per patient — will also apply to reni-cel, making equitable access a critical policy question for the approximately 100,000 Americans with sickle cell disease, most of whom are Black or Latino, a demographic that has faced persistent underinvestment in sickle cell research and treatment infrastructure for decades.

Frequently Asked Questions

Q: What were the RUBY Trial results?

A: 27 of 28 patients (96%) with severe sickle cell disease had zero painful sickle cell crises for up to two years after treatment with reni-cel. Their average hemoglobin levels rose to near-normal.

Q: How is reni-cel different from Casgevy?

A: Reni-cel uses CRISPR-Cas12a to edit the HBG1 and HBG2 fetal hemoglobin promoters directly. Casgevy uses CRISPR-Cas9 to target BCL11A. Both reactivate fetal hemoglobin but through different molecular pathways.

Q: Is reni-cel FDA-approved?

A: No. The RUBY Trial is Phase 1/2. FDA submission is expected based on these results. Casgevy is already FDA-approved and represents the current available option.

Q: How many Americans have sickle cell disease?

A: Approximately 100,000 Americans, disproportionately African American and Latino.

Q: Why is gene editing potentially better than bone marrow transplant for sickle cell?

A: Because patients use their own edited cells, eliminating the need for a matched donor and removing the risk of graft-versus-host disease — the immune attack that is the major complication of donor-based bone marrow transplants.

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June 13, 2026
Neuroblastoma in Children | CureSearch

It is a cancer that arises from immature nerve cells called neuroblasts. Neuroblastoma most often begins in the adrenal glands, which are located on top of the kidneys. However, tumors can form anywhere along the sympathetic nervous system, including the chest, neck, abdomen, or pelvis. In some children, the cancer is localized at diagnosis. In others, neuroblastoma has already spread to the lymph nodes, bone marrow, bones or liver.

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June 13, 2026
Which Beans Best Block the Spread of Cancer?

Which legumes are best at inhibiting the matrix metalloproteinase enzymes that allow cancer to become invasive?

Although we’re spending billions of dollars on fancy new types of chemotherapy, the overflowing sink that is cancer treatment is expected to rise by about 70% over the next two decades because drugs are being used to merely mop up the mess rather than turn off the faucet. You can’t really give drugs to people to prevent cancer because of the side effects and cost, but there is said to be “overwhelming…evidence that the dietary bioactive compounds found in whole plant-based foods have signiﬁcant anticancer and chemopreventive [cancer-preventing] properties.”

I’ve previously talked about the impact of diet and nutrition on the 10 hallmarks of cancer. The bottom line is that evidence points to a diet that includes minimal animal products and, perhaps more importantly, maximal plant foods. Some foods that seem to be especially beneficial include fruits (especially berries), vegetables (especially greens), legumes (beans, split peas, chickpeas, and lentils), nuts and seeds (especially flaxseeds), onions, garlic, mushrooms, herbs and spices (for example, turmeric), and, as a beverage, green tea.

Chemotherapy may not even be particularly good at mopping up the mess. “Cancer drugs often impair quality of life and fail to extend patient survival.” Let me say that another way: You’re paying for drugs—maybe selling your house to pay for drugs—that may just be making your life worse for no benefit. Some have suggested we demand at least three months of extended life from pharmaceuticals, but if we demand that chemo actually works, would companies give up testing new cancer drugs altogether? On the other hand, by requiring clinically important benefits—what a concept—maybe Big Pharma would reallocate resources toward targeting the more critical cancer processes like metastatic spread, since it’s the tumor metastasis that accounts for 90% of cancer-related deaths. Who cares if some drug shrinks your primary tumor if it’s spreading and cutting your life just as short?

What about controlling metastatic cancer with some of those natural bioactive compounds in plants? Evidently, “it has been proven that [plant] phytochemicals are able to inhibit nearly every step of the invasion-metastasis cascade,” at least in vitro (in a petri dish). Below is a list of some purported dietary sources of antimetastatic phytochemicals, which you can also see at 2:27 in my video Blocking the Cancer Metastasis Enzyme MMP-9 with Beans and Chickpeas.

All of these foods are shown to block all sorts of cancer-signaling pathways, but let me focus on one: matrix metalloproteinases (MMPs). Since about 90% of cancer disability and death is due to cancer spreading (metastasis), let’s talk about MMPs, which “actively participate in the whole metastatic journey.” Matrix metalloproteinases are enzymes that allow the cancer to tunnel through the surrounding flesh and invade the lymph or blood vessels, and then enable it to burrow in and grow somewhere else.

So, Big Pharma developed matrix metalloproteinase inhibitor drugs, which worked great in animal models but caused severe side effects in humans. So, what about using food? There are special proteins in legumes (beans, split peas, chickpeas, and lentils) that reduce MMP activity. But which is the leading legume? Researchers tested eight different kinds: lupin beans, chickpeas, split peas, black-eyed peas, lentils, more common beans (like kidney, black, or pinto), fava beans, and soybeans. Which do you think worked best?

Without any beans, the matrix metalloproteinase activity churned away at around 100%, and dripping on some protein from split peas didn’t seem to help much, but the black-eyed peas, lentils, common beans, and fava beans cut enzyme activity by more than 50%. Guess what slashed activity by more than 90%? Lupin beans, chickpeas, and soybeans, as you can see below and at 4:08 in my video.

But does this translate into slowing down the cancer’s spread?

Researchers plated a layer of human colon cancer cells in a petri dish and then took a razor blade to clear a strip down the middle. Within 48 hours, the cancer quickly converged to fill the gap. But when a little protein from lupin beans, chickpeas, or soybeans was dripped on, it looked like the cancer cells struggled to close the distance, as you can see below and at 4:33 in my video.

Okay, but they used raw beans. You don’t know if these anti-cancer proteins are destroyed by cooking until you put it to the test. Researchers found that the matrix metalloproteinase inhibitors in soybeans, at least, did remain active after cooking.

So, maybe it’s no wonder that eating legumes reduces the risk of colorectal cancer. Yes, but colon cancer, which sprouts from the inner lining of the colon, could potentially come in contact with some of these bean proteins. Presumably, they wouldn’t get into the bloodstream.

Those eating a vegetarian diet do seem to have significantly lower levels of matrix metalloproteinases, but this is just thought to be due to their lower levels of inflammation, similar to the way non-smokers also have lower MMP levels. This is good because this enzyme isn’t just a cancer biomarker, but also may be involved in autoimmune diseases and cardiovascular disease. The machete-type nature of this enzyme can hack through the inflamed, cholesterol-filled atherosclerotic lesions lining diseased arteries and cause the plaque to rupture. People know that those eating a more plant-based diet tend to have less heart disease, but may not realize they harbor significantly less cancer risk, too, particularly among those eating strictly plant-based diets.

Doctor’s Note

The video I mentioned is Fighting the Ten Hallmarks of Cancer with Diet.

For other videos on cancer metastasis, check the related posts.

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June 12, 2026
HHS Asks the Public What Works for Addiction Treatment in New Federal Request for Comment — Here Is Why It Matters

The U.S. Department of Health and Human Services published a Request for Information in the Federal Register on June 10, 2026, inviting public comment on which research, programs, and policies have been most successful in treating addiction, improving mental health outcomes, and supporting long-term recovery. The comment period runs through July 5, 2026, and is framed as part of HHS Secretary Robert F. Kennedy Jr.’s broader initiative, the administration has called the “Great American Recovery.”

The RFI arrives at a sobering moment for American public health. Opioid overdose deaths have remained above 70,000 annually since 2017 and exceeded 80,000 in 2024, making drug overdose one of the leading causes of death among Americans under age 55. Fentanyl and other synthetic opioids now account for the vast majority of these deaths. The toll extends far beyond mortality statistics — addiction devastates families, communities, workforce participation, and the children of people with substance use disorders.

The notice explicitly invites input from patients, people with lived experience of addiction and recovery, healthcare providers, community organizations, and researchers. The framing reflects a genuine uncertainty about the best path forward at the federal level — and, depending on how the administration responds to the comments received, could foreshadow significant shifts in federal drug and mental health policy.

What the Science Says About Addiction Treatment

The research base for addiction treatment has expanded substantially over the past two decades, and several evidence-based approaches have demonstrated consistent results. Medication-assisted treatment (MAT) for opioid use disorder — using buprenorphine (Suboxone), methadone, or naltrexone (Vivitrol) — remains the most extensively studied and most effective approach for reducing overdose deaths and helping patients maintain recovery. A landmark 2023 study in the New England Journal of Medicine found that patients receiving buprenorphine had significantly lower rates of overdose death than those who did not.

Despite this evidence, access to MAT remains severely limited. Fewer than 20 percent of people with opioid use disorder receive it, partly due to stigma, provider reluctance to prescribe, geographic disparities, and insurance barriers. Advocacy groups and harm reduction organizations have consistently pushed for more accessible prescribing, expanded availability in emergency departments, and removal of administrative barriers to buprenorphine.

Residential treatment, peer support specialists, contingency management (which uses positive reinforcement to promote drug-free behavior and is especially effective for stimulant use disorders), and community-based case management have all shown benefit in specific contexts. Mental health co-treatment is also increasingly recognized as essential, given that the majority of people with substance use disorders have co-occurring anxiety, depression, trauma, or other psychiatric conditions.

Harm reduction strategies — needle exchange programs, naloxone distribution, fentanyl test strips, supervised consumption sites — have a strong evidence base for reducing overdose deaths and HIV transmission, though they remain politically controversial and are not universally available.

What Advocates Want the Administration to Hear

Public health advocates are watching this comment process closely. Many are hoping the RFI signals a genuine commitment to expanding evidence-based treatment access rather than a pivot toward approaches that lack a strong scientific foundation. Questions about how the Kennedy-led HHS will address the scientific consensus on MAT, harm reduction, and the role of abstinence-only models will shape the federal response for years.

The comment process is open to all members of the public at federalregister.gov. Comments submitted by the July 5, 2026 deadline will inform HHS policy development.

Frequently Asked Questions

Q: What is the HHS asking for in this public comment request?

A: HHS is seeking input on which addiction treatment programs, policies, and research approaches have been most successful — to guide future federal policy and funding priorities.

Q: What are the most effective treatments for opioid use disorder?

A: Medication-assisted treatment (MAT) using buprenorphine, methadone, or naltrexone has the strongest evidence base. Combined with counseling and support services, MAT significantly reduces overdose deaths.

Q: How many Americans die of opioid overdoses each year?

A: Opioid overdose deaths exceeded 80,000 in 2024. Fentanyl and synthetic opioids now account for the vast majority of these deaths.

Q: How can I submit comments to the HHS RFI?

A: Comments can be submitted at federalregister.gov by the July 5, 2026 deadline.

Q: What is harm reduction and why is it controversial?

A: Harm reduction includes strategies like naloxone distribution, needle exchanges, and fentanyl test strips that reduce the risks of drug use without requiring abstinence. Evidence strongly supports their effectiveness, but they remain politically controversial in some settings.

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June 12, 2026
What Is Breast Cancer? – NCI

The female breast contains lobes, lobules, and ducts that produce and transport milk to the nipple. Fatty tissue gives the breast its shape, while muscles and the chest wall provide support. The lymphatic system, including lymph nodes, filter lymph and store white blood cells that help fight infection and disease.

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June 11, 2026
CDC June 2026 Health Outlook: COVID Summer Surge Risk, West Nile Early Season, and Salmonella Moringa Alert

Public health surveillance data released by the CDC as of June 5, 2026 offers a mixed picture of the nation’s current disease burden heading into the height of summer. COVID-19 activity is very low nationally, RSV and influenza seasons have ended, and the emergency department burden from respiratory illness is at its lowest point of the year. But officials are tracking several developing concerns that warrant attention from residents, clinicians, and travelers over the coming weeks.

COVID-19: Low Now, But a Summer Surge Is Possible in the South and West

The CDC’s June 5 Respiratory Virus Data update confirms that COVID-19 activity is currently very low across the United States, with declining hospitalizations nationally over recent months. As of June 2, the CDC estimates COVID-19 infections are declining or likely declining in 41 states and growing in only 1 state, according to the agency’s epidemic trend models.

However, the CDC’s 2026 COVID Summer Outlook specifically warns that regions which did not experience substantial COVID activity during the most recent winter months — particularly the South and West — are expected to see increases in summer. The pattern of summer COVID surges in these warmer regions has recurred in multiple years since 2020, driven by people moving indoors to escape heat and, in 2026, by the convergence of World Cup mass gatherings drawing large numbers of international visitors into cities across those exact regions.

People at higher risk of severe COVID outcomes — adults 65 and older, immunocompromised individuals, and those with significant underlying health conditions — should remain aware of updated vaccine recommendations and discuss antiviral treatment eligibility (Paxlovid) with their physician if they test positive.

West Nile Virus: An Unusually Early Season Beginning

West Nile virus activity has been confirmed earlier in the 2026 season than in most prior years, raising concern that peak summer transmission — which typically occurs July through September — could be more intense than average. Positive mosquito pools were confirmed in San Antonio in May (unusually early), in Frisco, Texas in early June, and in New Orleans in early June. Louisiana’s public health response included helicopter-based aerial spraying over parts of New Orleans and surrounding parishes. California confirmed positive mosquito samples across six counties by early June.

West Nile virus has no vaccine and no approved treatment. The CDC recommends using EPA-registered insect repellents containing DEET, picaridin, IR3535, or oil of lemon eucalyptus; wearing long-sleeved shirts and pants during peak mosquito hours (dusk to dawn); eliminating standing water around the home; and ensuring window and door screens are intact.

Salmonella in Moringa Supplements: 119 Cases, 36 States

The ongoing CDC alert on Salmonella in moringa leaf supplement products has expanded since initial publication in May 2026. As of the latest update, the outbreak has sickened at least 119 people in 36 states, hospitalized 32, and involves a drug-resistant strain of Salmonella linked to brands including Live it Up, TNVitamins, Doctor’s Pride, MOGO, and Why Not Natural. Anyone currently using a moringa supplement should check the FDA’s active recall list and stop use immediately if their product is on it.

Frequently Asked Questions

Q: What is COVID activity level in the U.S. right now?

A: As of June 5, 2026, COVID activity is very low nationally. CDC estimates infections are declining in 41 states. However, summer surges are possible in South and West regions.

Q: Is West Nile virus active this summer?

A: Yes. Positive mosquito pools have been confirmed earlier than usual in 2026 in San Antonio, Frisco TX, New Orleans, and six California counties. The early season start suggests potential for above-average transmission in peak summer months.

Q: What should I do about the Salmonella-moringa outbreak?

A: Stop using any moringa supplement and check FDA.gov/recalls for your brand. The outbreak has sickened 119 people in 36 states, with a drug-resistant Salmonella strain linked to several supplement brands.

Q: Who is most at risk from West Nile virus?

A: Adults 60 and older and immunocompromised individuals face the highest risk of neuroinvasive West Nile disease. About 80% of West Nile infections cause no symptoms; approximately 1% cause severe neurological illness.

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June 11, 2026
A Persistent Pesticide Is Linked to Alzheimer’s Risk

How can we avoid the breakdown products of pesticides that may increase the risk of Alzheimer’s disease as much as if you carried APOE e4, the so-called Alzheimer’s gene?

Although there is a growing list of Alzheimer’s disease susceptibility genes, those genes account for less than half of all Alzheimer’s cases. Here is the “single most compelling” piece of data on the potential control we have over the disease: When it comes to identical twins with the exact same genes, if one gets Alzheimer’s, the other usually does not. So, we have to think about all the other contributing factors beyond just genetics.

There’s a list of chlorinated pesticides, including DDE (a metabolite of DDT), that the U.S. Environmental Protection Agency has classified as probable human carcinogens. But in a study—which I’ve mentioned in a video on pesticides and cancer—blood levels of DDE and other pesticides were associated not with increased cancer mortality, but increased risk of other-cause mortality. This led researchers to speculate that this may be due to an associated increased risk of diabetes or dementia. I’ve talked previously about the diabetes link. What about dementia?

A research team at Rutgers found significantly higher blood levels of DDE in Alzheimer’s disease patients compared to controls, as you can see below and at 1:22 in my video Pesticides (DDT) and Alzheimer’s Disease.

Autopsy studies show blood levels are a good proxy for brain levels. Those patients with the highest levels were at about four times the odds of having dementia from Alzheimer’s. And in a petri dish, DDE increases amyloid precursor protein levels in human brain cells, providing a potential mechanism. Below and at 1:48 in my video, you can see the levels of the sticky protein implicated in the development of Alzheimer’s disease before and after DDE is added at the levels one finds circulating in highly exposed individuals among the general population.

Put all these studies together, and there does indeed seem to be a link, consistent with data showing about a doubling of risk for developing dementia among those acutely pesticide-poisoned, as you can see below and at 2:01 in my video.

Among U.S. elders, DDT and its breakdown product DDE are also associated with increased risk of cognitive decline in general, which is shown below and at 2:08 in my video.

DDT was used extensively in the United States from the 1940s through the early 1970s. At its peak, we were churning out about 180 million pounds a year. And it is still in our bodies to this day, contaminating the bloodstreams of more than 90% of Americans, with DDE—the pesticide linked to quadrupling the odds of Alzheimer’s—found at the highest levels of all.

It’s still in our bodies because it’s still in the food supply. In a previous video on the topic, I noted that the levels of DDT, DDE, and other banned pesticides and pollutants were much lower in the breast milk from a vegetarian mother compared to breast milk of her non-vegetarian sister. The largest difference was noted for DDE, which was four times lower in the vegetarian sister. This is what you see across the board for these kinds of pollutants. Below and at 3:20 in my video, you can see the levels of dioxins and PCBs found in beef, chicken, pork, processed meat, eggs, fish, dairy products, and all plant foods put together when food samples were collected from supermarkets across the United States.

These toxins build up in the food chain, so it makes sense that the most contaminated foods are meat, fish, and dairy products. The toxin levels were found to be 5 to 10 times higher in meat, eggs, fish, and dairy compared to plant foods. Unfortunately, cooking doesn’t destroy pollutants like DDE—in fact, it may make them even more concentrated. And this is for a pesticide that may increase the risk of Alzheimer’s disease as much as if you carried the so-called Alzheimer’s gene APOE e4.

Doctor’s Note

The video I mentioned is Pesticides and Cancer Risk.

For more videos on Alzheimer’s disease, check out the Alzheimer’s topic page.

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June 10, 2026
New York City Reports First Severe Mpox Clade I Case — A More Dangerous Strain Now Showing Up Across America

New York City has confirmed its first case of mpox caused by clade I — the more dangerous variant of the virus — raising concern among public health officials as the more infectious and more severe form of mpox continues to arrive in major U.S. cities. The NYC Health Department issued a formal advisory noting that there is no known local community transmission tied to this case, but health commissioner Dr. Alister Martin confirmed the virus is now present in the city and urged residents to be aware of symptoms and vaccination options.

As of May 9, 2026, the NYC Department of Health reported 79 mpox cases in New York City in 2026 alone, including at least a small number of clade I cases. Nationally, the CDC confirmed more than 20 clade I mpox cases in the United States as of June 2026, all linked to recent international travel or contact with travelers from affected regions in Central and Eastern Africa or Western Europe.

Clade I vs. Clade II: Why This Strain Is More Concerning

Most Americans became familiar with mpox during the 2022 global outbreak, which was caused by clade II — a less severe form of the virus with a survival rate above 99.9%. Clade I is different. According to Fox News senior medical analyst Dr. Marc Siegel, “Clade I causes more severe symptoms and can be life-threatening.” In the ongoing outbreak in the Democratic Republic of the Congo, clade I has had a case fatality rate significantly higher than clade II. Complications can include severe skin lesions, pneumonia, brain inflammation, and bacterial superinfections.

While clade I spreads through the same routes as clade II — primarily close physical contact, sexual contact, kissing, and contact with infected skin lesions or respiratory droplets at close range — it does not spread through casual airborne contact over long distances. The CDC has assessed the current risk to the general U.S. population as low, but characterizes the risk as low to moderate for men who have sex with men, who accounted for the majority of the 2022 U.S. outbreak.

Who Should Get Vaccinated and What to Watch For

The JYNNEOS vaccine, approved for mpox prevention, provides strong protection against both clade I and clade II. The CDC recommends the two-dose vaccine series for gay, bisexual, and other men who have sex with men aged 18 and older with specific risk factors. Anyone who traveled to or had contact with someone from the DRC, neighboring African countries, or parts of Western Europe reporting clade I cases should consult their healthcare provider immediately.

Symptoms of mpox typically appear 3 to 17 days after exposure and begin with fever, swollen lymph nodes, muscle aches, and exhaustion, followed by a distinctive rash that progresses through several stages of fluid-filled lesions. Anyone with a new or unexplained rash — particularly after recent travel or close physical contact — should contact a healthcare provider, mention any travel history, and avoid close contact with others until evaluated. NYC offers free mpox vaccination at multiple locations across the five boroughs.

The arrival of clade I mpox in New York City — the nation’s most densely populated metro area — is a reminder that the city’s international connectivity, while a source of enormous economic and cultural vitality, also serves as an entry point for emerging infectious diseases. Whether the public health infrastructure put in place after 2022 remains fully operational under reduced federal staffing is a question officials have not fully answered.

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June 10, 2026
Symptoms of ADHD | Attention-Deficit / Hyperactivity Disorder (ADHD)

Deciding if a child has ADHD is a process with several steps. There is no single test to diagnose ADHD, and many other problems, such as sleep disorders, anxiety, depression, and certain types of learning disabilities, can also have symptoms similar to ADHD.

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June 10, 2026