What are the pros and cons of Propecia and Rogaine for hair loss?
“Any consumer looking on the Internet for a treatment for hair loss is exposed to a multitude of remedies.” However, we only have good evidence for efficacy for drugs approved by the U.S. Food and Drug Administration: finasteride (sold as Propecia) and minoxidil (sold as Rogaine). It’s considered a myth that all the patented hair-loss supplements on the market will increase hair growth. And they may actually be more expensive, with over-the-counter supplement regimens costing up to more than $1,000 a year, whereas the drugs may cost between $100 and $300 annually. The drugs can help but can cause side effects. Propecia can diminish libido and cause sexual dysfunction, while the topical minoxidil can cause itching.
Below and at 1:12 in my video Pills for Hair Growth, you can see a list of some of the more common side effects of these FDA-approved drugs.
To understand why there are so many hormonal side effects for Propecia, like impotence, testicular pain, and breast enlargement, it’s important to understand how the drug works.
Androgens, male hormones like testosterone, are the principal drivers of hair growth in both men and women. We know this from studies half a century ago that show that castration of men stopped their hair loss. Why exactly were they being castrated? It was due to eugenics laws in the United States, when “mentally handicapped people” were castrated or forced to undergo tubal ligations against their will “to prohibit contribution to the genepool.” So-called “retarded persons were routinely sterilized without their consent or knowledge,” and the United States was the first country to introduce eugenic laws, which were later upheld by the U.S. Supreme Court. In the 1930s, a vocal proponent complained: “The Germans are beating us at our own game.”
Back to hair loss. Testosterone is the primary androgen circulating in the blood and can be converted to dihydrotestosterone, which is even more powerful, by an enzyme called5-alpha reductase, shown below and at 2:28 in my video.
That’s the enzyme that is blocked by Propecia, so it inhibits the souping up of testosterone. That’s why women are not supposed to take it since it could feminize male fetuses; whereas for men, it has sexual side effects like erectile dysfunction, which can affect them for years. It’s something the drug companies had to disclose for the last decade: a “difficulty in achieving an erection that continues after stopping the medication,” a side effect that may even be permanent. Up to 20% of study participants reported “persistent sexual dysfunction” for six or more years after stopping the drug, suggesting the possibility that it may be permanent.
It’s possible that the drug may structurally change the part of your brain responsible for sexual function. Indeed, though blood levels of hormones in users with persistent effects appear normal, analysis of the cerebrospinal fluid surrounding the brain, obtained via spinal tap, shows that neurosteroid levels do appear to end up being altered. So, “it is recommended that prescribers of finasteride, as well as potential users, be aware of the potential serious long-term risks of a medication used for a cosmetic purpose.”
To date, no new interventions are used routinely in treating male or female pattern baldness. Given the side effects of the current drug options, “there is a need for alternative treatments.” So, what about food? Could what we eat help combat hair loss? That’s exactly what we’re going to explore next.
Doctor’s Note
This is the second in a three-part series on hair loss and growth. Do Hair Growth Supplements Work?is the first video, in case you missed it.
Immune checkpoint inhibitors transformed melanoma treatment. They also leave a large share of patients behind, and figuring out what to do for those patients is the central unsolved problem in the field.
UCLA researchers have received a five-year, $3.9 million grant from the National Cancer Institute to work on it. The award goes to Cristina Puig-Saus, an associate professor of microbiology, immunology and molecular genetics and surgical oncology at the David Geffen School of Medicine and an investigator at the UCLA Health Jonsson Comprehensive Cancer Center, according to UCLA Health. She is also a member of the UCLA Broad Stem Cell Research Center and the UCLA Parker Institute for Cancer Immunotherapy.
This is funding for research, not a result. Nothing has been shown to help any patient, and the work described is preclinical.
The Grant Is About Fixing Non-Response, Not Explaining It
A distinction worth drawing precisely, because it changes what to expect from this work.
The project is not primarily a study of why some patients respond, and others do not. It is drug development aimed at overcoming barriers already identified. Using a drug screening platform developed in the Puig-Saus laboratory to test thousands of compounds, the team identified two candidates, and the two work by different routes.
One appears to strengthen the interaction between T cells and cancer cells, helping the immune system mount a more effective attack. The other makes tumor cells more susceptible to destruction by T cells without directly altering the immune cells themselves. That second approach is notable because it sidesteps the problem of a patient’s T cells being exhausted or scarce.
The funding will support testing whether those compounds boost the effectiveness of existing immunotherapies in preclinical melanoma models, investigating how the drugs work, and evaluating their potential to be used safely. Puig-Saus has said that because the compounds are designed to work alongside existing immunotherapies, the approach could potentially apply across many cancer types.
Why So Many Patients Do Not Respond
The underlying problem is worth explaining, because it is what any approach has to solve.
Checkpoint inhibitors work by releasing the brakes on T cells so they can attack tumors. That only helps if T cells can find the tumor in the first place. Two failure modes dominate.
The first is recognition. T cells often struggle to identify cancer cells, particularly when tumors reduce the display of the surface molecules that mark a cell as abnormal. A tumor the immune system cannot see is not helped by removing a brake.
The second is evasion. Tumors evolve under immune pressure. They can lose the specific proteins T cells were targeting, recruit suppressive cells, or create a local environment that exhausts T cells. Tumors described as cold have few infiltrating T cells to begin with.
The scale of the gap is substantial. UCLA has previously reported that 40 percent of patients with melanoma do not respond to checkpoint blockade, with response especially poor in rarer forms including acral melanoma on the palms and soles, uveal melanoma in the eye, and mucosal melanoma.
The Screening Platform Is the Method Worth Noting
How the two candidate compounds were found says something about where cancer drug discovery has moved.
Rather than starting from a hypothesis about a single molecule, the laboratory built a screening platform capable of testing thousands of compounds for effects on the interaction between T cells and cancer cells. That approach asks which compounds change the behavior of the system, then works backward to understand why.
The advantage is that it can surface candidates nobody would have predicted from existing biology. The trade-off is that a compound identified this way arrives without a fully worked-out mechanism, which is precisely why part of the grant is devoted to investigating how the drugs work rather than only whether they work.
That mechanistic question is not academic. Understanding how a compound acts is what allows researchers to predict side effects, identify which patients might benefit, and design sensible combinations with existing immunotherapies.
The Timeline for Anything Reaching Patients
Preclinical grants are frequently reported in ways that imply proximity to treatment, and the arithmetic does not support that.
Five years of preclinical work would be followed, if results justify it, by formal toxicology studies, manufacturing under regulated conditions, and an investigational new drug application before a first human trial. That first trial would test safety and dosing rather than benefit. Efficacy testing would follow.
Most compounds entering this pipeline do not reach patients. That is not pessimism about this particular project; it is the base rate, and it is why the honest framing is that federal funding has been committed to a promising question.
What patients with melanoma can act on is different. Checkpoint inhibitors, targeted therapies for BRAF-mutant disease, and tumor-infiltrating lymphocyte therapy are all available now depending on tumor characteristics and prior treatment. Molecular testing of the tumor determines which apply.
For patients whose disease has progressed on checkpoint inhibitors, clinical trials are frequently the most substantive option, and enrollment is concentrated at academic and NCI-designated cancer centers. The same laboratory is separately advancing an experimental CAR T cell therapy for melanoma toward a trial, which is the kind of option worth asking an oncologist about directly.
Melanoma prevention and early detection remain the most effective interventions available. Anyone noticing a mole that changes in size, shape, or color, has an irregular border or uneven color, or looks different from other moles should have it examined. Early-stage melanoma is frequently curable with surgery alone.
This article is general information and is not medical advice.
Frequently Asked Questions
What was funded? A five-year, $3.9 million National Cancer Institute grant to Cristina Puig-Saus at UCLA.
What will the money support? Preclinical testing of two compounds identified through a drug screening platform, aimed at boosting existing immunotherapies in melanoma models.
How do the two compounds differ? One strengthens the interaction between T cells and cancer cells. The other makes tumor cells more vulnerable to T cells without altering the immune cells.
Why do checkpoint inhibitors fail in some patients? T cells often cannot recognize cancer cells, and tumors evolve to evade immune attack. UCLA has reported that 40 percent of melanoma patients do not respond.
Has anything been shown to work? No. This is funding for research. No patient benefit has been demonstrated.
When could this reach patients? Not for many years, if at all. Preclinical work precedes toxicology, manufacturing, and first-in-human safety trials.
What can melanoma patients do now? Ask about molecular testing, currently approved options, and open clinical trials, particularly at NCI-designated centers.
The list of conditions that GLP-1 receptor agonists appear to protect against keeps getting longer. These drugs — which include semaglutide (Ozempic, Wegovy), tirzepatide (Mounjaro, Zepbound), and the newly approved orforglipron (Foundayo) — were originally developed for type 2 diabetes before emerging as transformative obesity medications. Then cardiovascular outcome trials showed they reduce heart attacks and strokes. Then the sleep apnea approval added obstructive sleep apnea to the indication list. Then studies suggested reductions in kidney disease progression, non-alcoholic fatty liver disease, and alcohol dependence.
And now, a major study presented at the American Society of Clinical Oncology Annual Meeting in Chicago in early June 2026 and reported widely on June 10, 2026 has added breast cancer to the rapidly expanding list of conditions that GLP-1 drugs appear to protect against — with an effect magnitude that has stunned the oncology community.
The study, which analyzed real-world data from a large cohort of women with type 2 diabetes or obesity who were treated with GLP-1 receptor agonists, found that GLP-1 drug use was associated with a 30 to 47 percent lower risk of developing breast cancer compared to women who did not use these medications. The lower end of that range (30 percent) emerged from analyses adjusted for body mass index and weight change — meaning even when researchers accounted for the weight loss that GLP-1 drugs produce, a significant protective signal remained. This finding strongly suggests that GLP-1 drugs may be protecting against breast cancer through mechanisms that go beyond simply reducing body fat — mechanisms that may include direct anti-tumor effects, reduced insulin resistance and associated growth factor signaling, or anti-inflammatory pathways.
Why This Finding Is Biologically Plausible
The biological connection between metabolic dysfunction, obesity, insulin resistance, and breast cancer risk is well established. Adipose tissue (fat) produces estrogen through a process called aromatization, making obesity a direct driver of estrogen-dependent breast cancers. Hyperinsulinemia — the elevated insulin levels that accompany insulin resistance in type 2 diabetes and obesity — activates the insulin-like growth factor (IGF-1) pathway, which promotes cancer cell proliferation and survival. Chronic inflammation from adipose tissue dysfunction activates oncogenic pathways that promote tumor growth.
GLP-1 receptor agonists address multiple of these pathways simultaneously. They reduce body fat (reducing aromatization and adipose inflammation), improve insulin sensitivity (reducing hyperinsulinemia and IGF-1 signaling), and have direct anti-inflammatory effects. Preclinical studies have also documented direct GLP-1 receptor agonist activity on cancer cell lines, suggesting GLP-1 receptors may be expressed in breast cancer tissue and may mediate direct anti-proliferative effects when activated.
The study’s finding that the protective signal persists even after adjustment for weight and BMI is the most provocative result, because it suggests the drug’s biological effects — beyond simple caloric restriction and fat mass reduction — are contributing to cancer protection.
What This Means for the 15 Million Americans on GLP-1 Drugs
Approximately 15 million Americans are currently prescribed GLP-1 receptor agonists. The vast majority are taking them for type 2 diabetes or weight management. If the breast cancer protective signal seen in this study is confirmed in larger prospective trials and in controlled analyses, it would represent an additional major health benefit of these medications — one that could influence prescribing decisions, insurance coverage arguments, and cancer prevention discussions.
The researchers caution that this is observational data from a real-world cohort, not a randomized controlled trial. Confounding variables — the possibility that GLP-1 drug users differ from non-users in ways that independently affect breast cancer risk — must be accounted for before these findings can be considered definitive. Prospective studies and potential randomized trials with cancer outcomes as endpoints are now being planned. The Phase 3 ORCA trial of semaglutide in high-risk cancer prevention populations is one ongoing effort that will provide higher-quality evidence.
For women currently taking GLP-1 drugs for any indication, this study is not a recommendation to take them as cancer prevention without diabetes or obesity indication — rather, it is an important signal that the health benefits of these medications may be broader than previously understood.
Frequently Asked Questions
Q: What did the new GLP-1 and breast cancer study find?
A: A real-world cohort study presented at ASCO 2026 found that women with type 2 diabetes or obesity who used GLP-1 receptor agonists had a 30–47% lower breast cancer risk compared to non-users. The effect persisted after adjustment for weight loss.
Q: Does this mean women should take GLP-1 drugs specifically to prevent breast cancer?
A: No. This is observational data, not a randomized trial. The finding is a promising signal that warrants further research, not a clinical recommendation for GLP-1 drugs as cancer prevention outside of established indications.
Q: Why might GLP-1 drugs protect against breast cancer beyond weight loss?
A: By reducing hyperinsulinemia, improving insulin sensitivity (lowering IGF-1 signaling), reducing adipose-tissue inflammation, and potentially through direct GLP-1 receptor activity on breast tissue — all mechanisms independent of weight loss.
Q: Which GLP-1 drugs were included in the study?
A: The study analyzed GLP-1 receptor agonist use broadly, including semaglutide (Ozempic/Wegovy) and tirzepatide (Mounjaro/Zepbound) among the most commonly used agents. Results were not limited to a specific drug within the class.
Q: How does this new finding fit with the other cancer data on GLP-1 drugs?
A: A 2024 Nature Medicine study documented lower incidence of multiple obesity-associated cancers in GLP-1 users. The 2026 ASCO breast cancer study adds specifically to that growing body of evidence suggesting GLP-1 drugs may have broad anti-cancer properties.
Blood pressure medications and lifestyle changes often work best when they are used together, especially for people who need long‑term BP control with antihypertensives and other hypertension drugs.
High blood pressure usually develops silently over years, so combining evidence‑based treatments with everyday habits helps lower numbers while also protecting the heart, brain, and kidneys. When both approaches are aligned, individuals have a better chance of reaching and maintaining healthy blood pressure targets.
Why Combine Blood Pressure Medications and Lifestyle Changes?
High blood pressure increases the risk of heart attack, stroke, kidney disease, and vision problems, even when a person feels fine. Antihypertensives and other hypertension drugs lower blood pressure through different mechanisms, such as relaxing blood vessels, reducing fluid volume, or slowing the heart rate.
Lifestyle changes, including diet, physical activity, and weight management, support these effects and can sometimes reduce the doses or number of medications needed.
When doctors suggest combining medication with lifestyle adjustments, they base this on blood pressure readings, other medical conditions, and overall cardiovascular risk.
Those with very high readings or organ damage usually need hypertension drugs promptly instead of relying on lifestyle changes alone. Over time, consistent BP control lowers the chance of serious complications and supports better long‑term health.
Main Types of Hypertension Drugs
There are several major classes of antihypertensives, and each type works in a different way. Physicians choose among these hypertension drugs based on age, other illnesses, possible side effects, and how high the blood pressure is at baseline. Often, more than one class is combined to achieve steady BP control.
ACE inhibitors block the formation of a hormone that narrows blood vessels, making it easier for blood to flow, and are frequently used in people with diabetes or kidney disease, according to the Centers for Disease Control and Prevention.
ARBs, or angiotensin receptor blockers, act on the same system but block the receptor, and they are often used when ACE inhibitors cause cough or are not well tolerated. Diuretics, or “water pills,” help the kidneys remove excess salt and water from the body, lowering blood volume and pressure and are often a first‑line option.
Calcium channel blockers relax the muscles in blood vessel walls and can be particularly helpful in some older adults and certain ethnic groups. Beta‑blockers reduce heart rate and the force of heart contractions, which can lower blood pressure and are especially useful when heart disease or certain arrhythmias are present.
Additional antihypertensives, such as aldosterone antagonists or fixed‑dose combination pills, may be used in resistant hypertension when standard treatments alone do not provide adequate BP control.
Can Lifestyle Changes Alone Control High Blood Pressure?
In some people with mild hypertension and no other major risk factors, lifestyle changes alone may be enough to bring blood pressure into a healthy range.
This is more likely when baseline readings are only slightly elevated and when individuals follow a structured plan closely. In many cases, however, lifestyle measures and antihypertensives work together rather than in place of each other.
A heart‑healthy eating pattern with plenty of fruits, vegetables, whole grains, and lean proteins supports BP control by improving blood vessel function and reducing excess sodium. Limiting salt intake, avoiding highly processed foods, and cooking more meals at home can meaningfully lower daily sodium levels.
Gradual weight loss, especially around the waist, and regular physical activity such as brisk walking, cycling, or swimming also contribute to lower blood pressure over time.
Limiting alcohol, avoiding tobacco, and managing stress with strategies like deep breathing, stretching, or mindfulness further assist BP control.
Even short daily activity, such as several five‑ to ten‑minute walks, can help those who cannot exercise for long periods. These lifestyle changes are recommended for everyone with elevated blood pressure, whether they take hypertension drugs or not.
Combining Antihypertensives and Lifestyle for Better BP Control
For many adults, the most effective strategy is to combine antihypertensives with practical lifestyle changes instead of relying on a single approach.
Hypertension drugs can bring levels down more quickly, which is important in preventing complications, while lifestyle habits help maintain these gains and may enhance the impact of the medications. This combined route often offers more flexibility in adjusting doses and tailoring treatment over time.
Monitoring is central to good BP control. Home blood pressure monitors allow individuals to track readings between clinic visits and show how well antihypertensives and lifestyle changes are working together.
Recording readings at consistent times, such as morning and evening before medications or meals, gives a clearer picture than occasional checks alone.
Regular follow‑up with a healthcare professional helps review averages, address side effects, and adjust doses or add new medications when needed. Blood and urine tests may be used to check kidney function and electrolyte levels, especially when certain drug classes or higher doses are used.
Over time, this careful monitoring supports a personalized mix of hypertension drugs and lifestyle strategies that best fit each person’s health profile and preferences.
Side Effects, Adherence, and Long‑Term BP Control
Like all medications, antihypertensives can cause side effects, although many are mild and manageable. Some people notice dizziness, fatigue, frequent urination, or ankle swelling, depending on the drug class.
Reporting these symptoms allows clinicians to adjust the dose, change timing, or switch to a different hypertension drug when appropriate.
Lifestyle choices can sometimes ease or reduce the impact of minor side effects, such as staying hydrated, rising slowly from sitting or lying, and maintaining gentle, regular physical activity.
Individuals are generally advised not to stop antihypertensives on their own, since abrupt changes can destabilize BP control and raise health risks. Tools like pill organizers, smartphone reminders, and written logs can support daily medication use and help people stay on track.
Long‑Term Heart Health With Antihypertensives and Lifestyle Changes
For those living with high blood pressure, viewing antihypertensives and lifestyle changes as partners can reshape how BP control is approached.
Hypertension drugs provide a reliable way to lower numbers and reduce immediate cardiovascular risk, while diet, movement, weight management, and stress reduction strengthen those effects and support overall heart health.
When both elements are built into daily routines and reviewed regularly with a healthcare professional, many people are better able to reach stable BP control, protect vital organs, and maintain healthier lives over the long term.
Frequently Asked Questions
1. Can blood pressure return to normal after starting antihypertensives?
Yes, many people reach target BP with antihypertensives plus lifestyle changes, but they usually need ongoing treatment to keep levels in a healthy range.
2. Is it safe to take antihypertensives at night instead of in the morning?
Timing can be adjusted, but it should be done under medical guidance; some people benefit from evening dosing, while others do better with morning schedules.
3. Do all hypertension drugs cause weight gain or fatigue?
No, side effects vary by drug class and person; if weight or energy changes appear, doctors can often switch or adjust medications.
4. Can someone with controlled BP ever stop taking hypertension drugs?
Sometimes, after sustained control and major lifestyle improvements, doctors may carefully taper doses, but stopping is never recommended without supervision.
What happened when topical olive oil was pitted against an ibuprofen-type drug for osteoarthritis and rheumatoid arthritis?
Fifty million Americans suffer from arthritis, and osteoarthritis of the knee is the most common form, making it a leading cause of disability. There are several inflammatory pathways that underlie the disease’s onset and progression, so various anti-inflammatory foods have been put to the test. Strawberries can decrease circulating blood levels of an inflammatory mediator known as tumor necrosis factor, but that doesn’t necessarily translate into clinical improvement. For example, drinking cherry juice may lower a marker of inflammation known as C-reactive protein, but it failed to help treat pain and other symptoms of knee osteoarthritis. However, researchers claimed it “provided symptom relief.” Yes, it did when comparing symptoms before and after six weeks of drinking cherry juice, but not any better than a placebo, meaning drinking it was essentially no better than doing nothing. Cherries may help with another kind of arthritis called gout, but they failed when it came to osteoarthritis.
However, strawberries did decrease inflammation. In fact, in a randomized, double-blind, crossover trial, dietary strawberries were indeed found to have a significant analgesic effect, causing a significant decrease in pain. There are tumor necrosis factor inhibitor drugs on the market now available for the low, low cost of only about $40,000 a year. For that kind of money, you’d want some really juicy side effects, and they do not disappoint—like an especially fatal lymphoma. I think I’ll stick with the strawberries.
One reason we suspected berries might be helpful is that when people consumed the equivalent of a cup of blueberries or two cups of strawberries daily, and their blood was then applied to cells in a petri dish, it significantly reduced inflammation compared to blood from those who consumed placebo berries, as you can see below and at 2:02 in my video Extra Virgin Olive Oil for Arthritis.
Interestingly, the anti-inflammatory effect increased over time, suggesting that the longer you eat berries, the better. Are there any other foods that have been tested in this way?
Researchers in France collected cartilage from knee replacement surgeries and then exposed it to blood samples from volunteers who had taken a whopping dose of a grapeseed and olive extract. They saw a significant drop in inflammation, as shown below and at 2:30 in my video.
There haven’t been any human studies putting grapeseeds to the test for arthritis, but an olive extract was shown to decrease pain and improve daily activities in osteoarthritis sufferers. So, does this mean adding olive oil to one’s diet may help? No, because the researchers used freeze-dried olive vegetation water. That’s basically what’s left over after you extract the oil from olives; it’s all the water-soluble components. In other words, it’s all the stuff that’s in an olive that‘s missing from olive oil.
If you give people actual olives, a dozen large green olives a day, you may see a drop in an inflammatory mediator. But according to a systematic review and meta-analysis, olive oil—on its own—does not appear to offer any anti-inflammatory benefits. What about papers that ascribe “remarkable anti-inflammatory activity” to extra virgin olive oil? Their evidence is from rodents. In people, extra virgin olive oil may be no better than butter when it comes to inflammation and worse than even coconut oil.
So, should we just stick to olives? Sadly, a dozen olives could take up nearly half your sodium limit for the entire day, as you can see below and at 3:47 in my video.
When put to the test, extra virgin olive oil did not appear to help with fibromyalgia symptoms either, but it did work better than canola oil in alleviating symptoms of inflammatory bowel disease. Unfortunately, I couldn’t find any studies putting olive oil intake to the test for arthritis. But why then is this blog entitled “Can Olive Oil Compete with Arthritis Drugs?” Because—are you ready for this?—it appears to work topically.
Topical virgin olive oil went up against a gel containing an ibuprofen-type drug for osteoarthritis of the knee in a double-blind, randomized, clinical trial. Just a gram of oil, which is less than a quarter teaspoon, three times a day, costing less than three cents a day, worked! Topical olive oil was significantly better than the drug in reducing pain, as you can see below and at 4:37 in my video.
The study only lasted a month, so is it possible that the olive oil would have continued to work better and better over time?
Is olive oil effective in controlling morning inflammatory pain in the fingers and knees among women with rheumatoid arthritis? The researchers went all out, comparing the use of extra virgin olive oil to rubbing on nothing and also to rubbing on that ibuprofen-type gel, and, evidently, the decrease in the disease activity score in the olive oil group beat out the others.
Doctor’s Note
For more on joint health, see related posts below.
A naturally occurring hormone in our body, glucagon-like peptide-1 (GLP-1) plays a role in regulating our blood sugar, appetite, and digestion. Our gastrointestinal tract releases more than 20 different peptide hormones, including GLP-1. The primary stimuli for secreting GLP-1 are meals rich in fats and carbohydrates, and GLP-1’s main action is to signal satiety to the brain. It also slows our digestion. Delaying the rate at which food leaves our stomach not only helps us feel fuller for longer, but also helps with our blood sugar control. When GLP-1 or an agonist (mimic) is dripped into people’s veins, appetite is reduced, leading to markedly reduced food consumption—a decrease in caloric intake by as much as 25 to 50 percent.
About GLP-1 Drugs
Our GLP-1 hormone acts as an appetite suppressant by targeting parts of the brain responsible for hunger and cravings. GLP-1-secreting cells don’t only line our intestines; they’re also in our brains. These new anti-obesity drugs are GLP-1 agonists, mimicking the hormone’s action by binding to GLP-1 receptors.
Our body breaks down GLP-1 so quickly that it hardly makes it even one time around our circulatory system, which is why we can’t just take the hormone directly. A compound was discovered—in the venomous saliva of a lizard called the Gila monster—that mimics GLP-1 but is resistant to breakdown. Using that compound as a template, the first GLP-1 agonist was created and approved for the treatment of diabetes about 20 years ago. Instead of most of it being cleared from the body within two and a half minutes, like native, natural GLP-1, much of the drug remains in the body for two and a half hours. That still means twice-daily injections, though, so then came liraglutide, which lasts all day.
What Is Ozempic?
Eventually, semaglutide was developed and branded as Ozempic, which could be injected just once a week. Ozempic was approved in 2017 to treat diabetes. Within a few years, a daily oral version had been developed, again for diabetes, but researchers running those clinical trials noticed a surprising side effect: People’s appetites diminished.
How Does Ozempic Work?
In a way, GLP-1 agonist drugs work like birth control pills. The Pill mimics placental hormones, thereby tricking our body into thinking we’re pregnant all the time. Ozempic-type drugs mimic GLP-1, thereby tricking our body into thinking we’re eating all the time. That’s how it dials down our hunger drive.
Ozempic for Weight Loss
In the longest trial to date, more than 17,000 individuals were randomized to injections of either high-dose semaglutide or placebo for four years. Overall, those on the drug lost 9 percent more body weight than those in the placebo group, but all the weight was lost in the first 65 weeks. Even though they continued to get injected every week for three more years, they didn’t lose any more weight over the subsequent 143 weeks.
Weight loss tends to plateau because the same amount of effort to cut calories—whether through willpower, drugs, or surgery—is met with growing resistance as ongoing weight loss increasingly activates our feedback control circuit, stimulating our appetite. In the case of the GLP-1 drugs, the weight loss caused by the initial drop in appetite is undercut by an apparent exponential increase in caloric intake as our body ratchets up our hunger again. Within 12 months, this resistance, combined with the decreased caloric needs from being lighter, matches the persistent effort to cut calories, and weight loss plateaus. And, as soon as we stop taking the drugs, our full appetite resumes and we start regaining the weight we initially lost.
The Cost of Ozempic
Wegovy, the high-dose Ozempic used for weight loss, costs up to $1,350 a month, which, again, may have to be paid in perpetuity since any lost weight can pile back on if you stop taking it. So, that could cost more than $16,000 a year if paid out-of-pocket for those whose insurance doesn’t cover it.
Ozempic Side Effects
The most common side effects include nausea, vomiting, diarrhea, and constipation. Gallbladder issues are another side effect; excess cholesterol shed from fat cells can crystalize in our bile like rock candy, forming gallstones.
Rare but serious adverse effects are also emerging. The package inserts for both semaglutide and tirzepatide list a series of “warnings and precautions” that include thyroid tumors, acute inflammation of the pancreas (pancreatitis), acute gallbladder disease, acute kidney injury (that may stem from dehydration due to excess vomiting or diarrhea), allergic reactions, a heightened risk of bottoming out blood sugars while on blood sugar–lowering medications, worsening eye disease for those with type 2 diabetes, an increase in heart rate requiring monitoring, and suicidal thoughts and behaviors.
What Is “Ozempic Face”?
“Ozempic face” is a term used to describe a distorted facial appearance among users of the drug. (Similar accounts have been made of “Ozempic butt.”) Media reports have linked the drug with facial aging, but the sagging appearance has been ascribed simply to the accelerated loss of fat in the face. While this interpretation seems logical, a review of the phenomenon concluded that “this explanation cannot fully account for the markedly accelerated facial aging….” Other factors suspected as being responsible for the appearance of premature facial aging include the loss of facial muscle mass, diminished structural integrity of the skin, and changes in stem cell function and hormonal secretion.
Is Ozempic Safe?
In the first quantitative benefit-versus-harm balance analysis, the researchers concluded that those achieving a 10 percent weight loss had a more than 90 percent chance that the benefits of taking the drugs outweigh the harms, but the opposite was found for individuals achieving only a 5 percent weight loss.
At this time, we don’t know about the long-term harms or benefits because some of these drugs and dosing schedules are so new. To complicate matters, the American Academy of Pediatrics has suggested offering these drugs for teens and even tweens as young as age 12. These drugs work by acting on the brain, so who knows what effect they might have on childhood development and beyond if young people end up taking them for the rest of their lives. Although we now have evidence of near-term benefit over a few years, we cannot assume long-term safety until it has been demonstrated.
Ozempic Alternatives
We don’t need to take GLP-1-mimicking drugs. Not only can the ingestion of a plant-based meal more than double GLP-1 secretion, compared to a meat meal, but plant-based diets can also cause weight loss by boosting our resting metabolic rate and incorporating “calorie-trapping” high-fiber foods that flush calories away. The largest study of people eating strictly plant-based found they are about 35 pounds lighter on average.
When we eat a donut, its fat, sugar, and starch get absorbed quickly, high up, before reaching the part of our digestive tract where we produce most of the hormone that suppresses our appetite, GLP-1. Since the cells that produce GLP-1 in response to calorie exposure are concentrated at the end of our digestive tract, while the majority of the calories we consume are absorbed early on, most calories never make it down far enough. That’s why our appetites aren’t suppressed very much these days. From a GLP-1 standpoint, when we have that donut, it’s like we never ate much of anything. No wonder we reach for donut number two.
Our prehistoric ancestors are believed to have consumed as much as 100 daily grams of fiber, which is more than six times what most of us are getting these days. We evolved eating massive amounts of whole plant foods—the only places fiber is found in abundance. That enabled out natural satiety mechanisms to keep us from overeating. By eating the way nature intended, we can release GLP-1 the way nature intended. That helps explains why in the medical literature, compared to any other way of eating that didn’t involve portion control, a whole food, plant-based diet has been shown to lead to greater average weight loss than any other diet.
For more in-depth information on Ozempic and GLP-1, check out these resources:
Popular weight loss and diabetic medications with semaglutide could help tobacco smokers quit smoking, a recent study revealed.
The researchers made the interesting finding after examining medical records of more than 200,000 new users of antidiabetes medications, including around 6000 people who started semaglutide drugs such as Ozempic and Wegovy.
Apart from semaglutide drugs, other antidiabetic medications studied were insulin, metformin, dipeptidyl-peptidase-4 inhibitors, sodium-glucose cotransporter-2 inhibitors, sulfonylureas, thiazolidinediones, and other GLP-1RAs.
During the study, researchers investigated whether individuals with tobacco use disorder who were on any of these antidiabetic medications received prescriptions for smoking cessation or were referred to counseling during their medical visits. After a follow-up for a year, researchers noticed a reduction in both medication prescriptions and counseling referrals in those who used semaglutide drugs.
The results published in the journal Annals of Internal Medicine indicate that the smoking cessation effect was strongest within 30 days of starting semaglutide. However, the effect continued for about 180 days before it leveled off.
“Semaglutide was associated with lower risks for tobacco use disorder-related health care measures in patients with comorbid type 2 diabetes mellitus and tobacco use disorders compared with other antidiabetes medications, including other GLP-1Ras, primarily within 30 days of prescription,” the researchers wrote in the study.
Although the study was observational and did not track factors such as actual tobacco use, cravings, or smoking cessation, the researchers consider their findings significant. They point out that cigarette smoking remains the top cause of preventable disease and death, and making any progress toward effective prevention is a hopeful step forward.
However, the researchers caution that their findings are too preliminary to suggest prescribing semaglutide drugs for smoking cessation, and more research is required to estimate the effects of semaglutide in the treatment of tobacco use disorder.
The study has not evaluated the exact mechanism by which semaglutide helps curb smoking. However, earlier studies suggest that it has to do with the drug’s effect on the brain’s reward system.
A similar recent study published in the journal Nature Communications has established a link between the use of semaglutide drugs and a reduction in alcohol use disorder. The study shows around 50%-56% reduced risk for both the incidence and recurrence of alcohol use disorder in semaglutide users during a 12-month follow-up.
That’s the enzyme that is blocked by Propecia, so it inhibits the souping up of testosterone. That’s why women are not supposed to take it since it could feminize male fetuses; whereas for men, it has sexual side effects like erectile dysfunction, which can affect them for years. It’s something the drug companies had to disclose for the last decade: a “difficulty in achieving an erection that continues after stopping the medication,” a side effect that may even be permanent. Up to 20% of study participants reported “persistent sexual dysfunction” for six or more years after stopping the drug, suggesting the possibility that it may be permanent.
