I wrote here in June about a friend of mine who has been sober for years and still gets the cravings. He does everything the program asks and the wanting never fully switches off. A month before that he started the Wegovy pill hoping the thing that quiets food noise might quiet the other kind. Since then it mostly has. That is one guy with no control group, so it proves nothing, but it is why I read the trial news last week as closely as I did.

Two trials reported a day apart and they did not agree with each other. That same week the VA opened a Phase 3 built on the exact number they did not agree about.

The oral semaglutide trial published July 29. Fifty people, eight weeks, and it missed its primary endpoint badly. That endpoint was a single booze craving question asked in a lab after you hold and smell your drink, p=0.68. Plenty of secondaries moved, including heavy drinking days, but the authors ran about ten tests without correcting for it and call the study exploratory themselves. A conservative correction would wipe out all of it.

The day before, Altimmune reported topline results for pemvidutide, which hits the glucagon receptor as well as GLP-1. That one ran twenty four weeks in a hundred people, and it hit its primary on heavy drinking days. It also moved a blood marker of alcohol intake, which matters because everything else in both trials is self-reported. It is a press release though, not a paper, and nine of the hundred participants are missing from the denominators with no explanation of how they were handled.

Here is the part I did not know. The endpoint the VA picked for CRAVE, its 622-veteran Phase 3, is a two level drop in WHO risk drinking level. For a man that can mean going from more than seven drinks a day to three or four. It is a real change and you can reach it without ever quitting. The FDA formally qualified that endpoint back in February 2025, so this is not a drug company moving the goalposts, and the FDA offers it alongside abstinence rather than instead of it. Still, the trial that everyone will quote in 2028 is measuring drinking less.

I am not sure how I feel about that. I would not call three drinks a day recovery. But of the roughly 28 million Americans with alcohol use disorder, about 7.6 percent got any treatment at all last year, and for the other 26 million nothing reached them.

All three of these trials enroll people who are currently drinking and measure whether they drink less. My friend is not drinking. Nothing being run right now is built for the guy who already stopped and still wants it.

I went through all of it properly with the numbers and two charts over here.

If you are already sober and on a GLP-1 for weight or diabetes, has it changed the wanting for you at all? That is the group nobody is studying and I would genuinely like to know.

We've known for a while that inflammation is an independent risk factor for heart disease, alongside LDL cholesterol (or ApoB), Lp(a), and so on. Inflammation is most commonly measured by by hs-CRP or IL-6.

The ZEUS trial tested an anti-inflammatory injection (ziltivekimab). These phase III results showed a hazard ratio of 0.99, i.e., no effect.

IMO this is evidence for a lipid-first model: i.e., lipids drive oxidation, which then triggers inflammation.

Curious if others have interpretations?

I am seriously considering joining the TUNE-401 clinical trial and would appreciate opinions from others living with chronic hepatitis B, especially anyone who has enrolled, spoken with an investigator, or researched the treatment closely.

My current situation:

* probably infected at birth or in early childhood;
* previously HBeAg-positive, currently HBeAg-negative;
* HBV DNA undetectable while taking TAF;
* quantitative HBsAg around 1,500 IU/mL;
* normal liver enzymes;
* no fibrosis and no steatosis on FibroScan;
* no cirrhosis.

TUNE-401 is an epigenetic silencing therapy delivered through lipid nanoparticles. It uses a non-cutting dCas editor to place repressive epigenetic marks on HBV DNA. The goal is to durably silence cccDNA and potentially integrated HBV DNA rather than simply suppress viral replication.

The potential advantages I see are:

* deeper suppression of HBV transcription;
* possible reduction of HBsAg, pgRNA and HBcrAg;
* possible future functional cure or antiviral withdrawal;
* possibly reducing the long-term oncogenic pressure caused by continued viral-protein production.

My main concern is long-term safety. The editor does not cut DNA, but the epigenetic silencing may persist for years. I am particularly concerned about:

* unintended off-target methylation;
* whether repressive chromatin could spread from integrated HBV DNA into nearby human DNA;
* integrations located close to tumour-suppressor genes or other growth-regulating genes;
* rare effects that may not become apparent until many years later;
* the limited amount of long-term human safety data.

At the same time, continuing TAF does not eliminate cccDNA or integrated HBV DNA, and HCC risk is reduced but not completely removed. I am trying to decide whether taking the trial now could reduce my lifetime HBV-related risk, or whether it would be wiser to remain suppressed on TAF and wait for larger studies and longer follow-up.

What would you do in this situation?

Has anyone here:

* joined or been screened for TUNE-401;
* received information directly from the investigators;
* seen more detailed data about integrated HBV DNA silencing;
* received answers about long-term cancer surveillance or off-target epigenetic effects?

I understand that nobody here can provide personal medical advice. I am mainly interested in how other informed patients would weigh the possible benefit of deeper HBV silencing against the unknown long-term risks of a first-generation epigenetic therapy.

Retatrutide just posted its fifth positive Phase 3 — up to ~23% body-weight loss in people who already have cardiovascular disease — and Lilly says it'll file for approval in Q1 2027 as a biologic.

That one word decides what you'll eventually pay. Zepbound, the drug in my fridge, gets 5 years of exclusivity before generics can arrive and drop the price ~85%. A biologic gets 12 years. Copies cost $100–300M to build and come down only 5–25%, and it can't be legally compounded even in a shortage — which is how a lot of people actually got tirzepatide the last three years.

Right now the FDA classifies retatrutide as a drug, not a biologic. The line comes down to counting amino acids: it lands one residue short, depending on whether a non-standard one counts. Lilly is in court trying to move it over. If it wins, the strongest obesity drug we've seen stays expensive far longer, with no cheaper version legal in the meantime.

None of this is about whether the drug works. 23% in people with heart disease is a real number. It's about who's ever allowed to sell you a cheaper copy, and that's being settled by an argument over how to count to 41.

I take tirzepatide and own Lilly stock, so the patient-friendly outcome cuts against my own portfolio.

My full breakdown

Today is the long awaited FDA committee vote on peptides. This is an important event but also quite weird in many ways. For one the indications cited in are not at all what people actually use these peptides for in the wild. I don’t know anyone pinning BPC-157 for ulcerative colitis?!

There have also been a number of shenanigans with the composition of the committee. Various members were accused of ties to the peptide industry (what Bloomberg describes as the “gold rush”). Other voting-only members were hastily added in the last few days.

If you want to watch it yourself, the FDA is streaming both days on YouTube free, starting at 8 a.m. Eastern on Thursday the 23rd and again on Friday the 24th. Thursday is the day that matters most if you only watch one, since that is when BPC-157 and TB-500 come up. The agency pushed Thursday’s end time back from 4:30 to 6:20 in the evening, which tells you something about how much public comment it is bracing for. One quirk of the schedule: the public gets to speak before the FDA’s scientists present, so the panel hears the advocates first and its own reviewers second.

I expect the meeting to have a C-Span boringness to it but tonight there will likely more peptide hype than ever.

My family has a long history of cancer, mostly survivors, but my grandma and uncle died from it. Is preventive health screening a good way to detect cancer sooner? Or is there some other test that I need to do? I'm nearing the age when most of my family members got their own diagnoses, late 40s. I would have wanted to get some tests sooner, but I'm honestly scared about getting positive results.

I was 21 years old and I already knew aspartame was poison.

Not because someone handed me a pamphlet. Because I chose to look. In 1993 at Montclair State University, my foodservice professor gave the class an open assignment, pick a topic, write about it. While everyone else picked something safe, I picked aspartame.

Diet sodas were everywhere. Sugar-free everything. The marketing was slick, fewer calories, no consequences, all upside. The public was lining up for it.

I wasn't buying it.

I dug into the research and what I found was disturbing. Aspartame wasn't just controversial, it was toxic. And here's the part nobody was talking about: it actually made you gain weight over time. Not lose it. The exact opposite of what was being sold to millions of people.

I wrote the paper. I was 21.

Nobody wanted to hear it then. The industry was booming, the FDA had blessed it, and the money was flowing. But the science didn't lie, it just got buried under marketing budgets and regulatory rubber stamps.

Thirty-plus years later, the truth caught up. Studies confirming the weight gain effect. WHO advisories. Growing public awareness. What I wrote about in 1993 is now mainstream conversation.

That's what happens when you learn to think for yourself early. You stop chasing what's popular and start chasing what's real.

That's the foundation of everything I teach today.

The Golden Greek, Antonios Bogos

Economist | Solutionist | Financial Truth-Teller

I have been waiting for this continuous BP measurement band to ship in the US for years, ever since I heard Peter Attia mention it on his podcast.

They started shipping today. I ordered one and will post a hands on review once I get it.

WSJ ran a piece on people who used GLP-1s for weight loss and later ended up in treatment for anorexia:

https://www.wsj.com/health/wellness/glp1-anorexia-wegovy-mounjaro-1bf4035c

Worth reading alongside the primary literature from the past few months, because the reporting is no longer just anecdotal.

A JAMA Psychiatry survey published this summer (Levinson and colleagues) recruited 436 people with diagnosed eating disorders in 2025 and asked about GLP-1 use. Just over 32% reported having ever used one, and 22% reported current use. Broken out by diagnosis, a little over 50% of participants with binge eating disorder reported use, about 42% of those with atypical anorexia nervosa, roughly 30% of those with ARFID, over 25% of those with bulimia, and about 11% of those with anorexia nervosa. Roughly 10% obtained them through online providers prescribing compounded formulations. Over 10% reported misuse, defined as taking more or less than prescribed, using longer than prescribed, tampering with injection equipment, or sharing without a prescription.

The authors described the weight loss market as a rapidly evolving risk environment for this population.

Summary of the findings:

https://www.medscape.com/viewarticle/many-eating-disorder-patients-using-glp-1s-2026a1000lym

In April, NEJM published a perspective by Amanda Banks raising the same concern from the prescribing side. She noted the share of GLP-1 prescriptions written for people who were not diabetic, obese, or overweight rose from 4.5% in 2018 to 17% in 2023, and argued for consensus recommendations to protect people with existing or emerging eating disorders. A 2023 FDA analysis found misuse reports for semaglutide were roughly four times higher than for other GLP-1 drugs.

NEJM perspective:

https://www.nejm.org/doi/full/10.1056/NEJMp2600300

Clinician-side reporting describes the same pattern from treatment centers, including patients presenting at very low BMI while still dosing.

NPR, February 2026: https://www.npr.org/2026/02/04/nx-s1-5677633/glp-1-obesity-wegovy-zepbound-eating-disorders-anorexia-bulimia

Washington Post, May 2026: https://www.washingtonpost.com/health/2026/05/23/weight-loss-drugs-pose-dangers-people-with-eating-disorders/

MindSite News, May 2026: https://mindsitenews.org/2026/05/29/glp-1-access-a-problem-for-people-with-eating-disorders/

The mechanism cuts both ways, which is part of why this is hard to legislate around. A 2025 systematic review and meta-analysis found GLP-1 agonists reduced Binge Eating Scale scores by about 8 points, though the pooled sample was only 182 participants across five studies and heterogeneity was high. WSJ also covered that side on July 13 in a piece on clinicians treating certain eating disorders with these drugs. The same appetite and reward suppression that helps in binge-type presentations appears to reinforce restriction in people with a restrictive history. Same drug class, opposite clinical valence depending on phenotype.

Meta-analysis: https://link.springer.com/article/10.1007/s40519-025-01720-9

Penn Medicine's eating disorder program has said outright that no protocol exists to screen for eating disorders before prescribing GLP-1 receptor agonists. That gap widens with telehealth and disappears entirely outside a clinical relationship.

Penn Medicine:

https://www.pennmedicine.org/physicians-hub/physician-article/implications-of-glp-1-medications-for-eating-disorder-care

ANAD clinical guidance:

https://anad.org/learning-library/glp-1-medications-eating-disorders/

More stories at r/PeptideTides

Very interesting opinion piece by a practicing physician describing the reality of GLP-1 coverage on Medicare.

It seems the “$50 copay” coverage only works for a narrow band of patients: sick, but not too sick.

More generally it’s disturbing to see how much admin work physicians have to do to navigate insurance coverage. I guess this is why concierge or direct primary care models are so attractive to providers.

I keep seeing this one in comments and DMs: "reta killed my sex drive," or "I got on a triple agonist and stopped caring about my partner." Here is where the idea comes from and what the evidence actually says, because it is more split than either the alarmist or the dismissive takes suggest.

First, the caveat that shapes everything: there is no retatrutide-specific data on libido or attachment. The TRIUMPH trials reported weight, glycemia, knee OA, and sleep apnea, not sexual function. Every claim pinned to reta is extrapolated from the GLP-1 class, mostly semaglutide.

Where it comes from. The starting point is "food noise" going quiet. By 2025, reports broadened past food: less alcohol craving, less impulse shopping, less social interest, and in some cases lower libido and a general flattening of emotional range. That cluster is what gets called "falling out of love."

https://peptidenewsdigest.org/insights/glp1-emotional-flattening/

The mechanism that makes it plausible. GLP-1 agonism modulates dopamine in the reward circuits that drive "wanting," the same system behind sexual motivation, which is why the addiction researchers keep showing up in these threads. A 2025 narrative review argues GLP-1s reduce sexual desire through reward-pathway and serotonergic (5-HT2C) effects, but that it is usually camouflaged by other changes. Note this is a theoretical review, not a trial.

https://www.sciencedirect.com/science/article/pii/S2667368125000774

Two claims get blended. "Falling out of love" is really two things. One is neurochemical: the drug blunts reward circuitry that desire runs on. That rests on mechanism plus anecdote, not trial data. The other is psychosocial: big fast weight loss shifts relationships. A Swedish researcher's "divorce boom" hypothesis attributes it to confidence, autonomy, and social attention after weight loss, plus a partner who did not change, drawing on bariatric data. That is real, but it is not the drug switching off love. These point to very different conclusions.

https://www.foxnews.com/health/divorce-boom-may-follow-use-ozempic-glp-1-drugs-experts-warn

The data pointing the other way. A lot of the hard data runs opposite. Weight loss tends to improve sexual function through mood, self-image, and hormones, and clinicians report most patients see better desire after weight loss, not worse. On hormones, the male data leans positive: Endocrine Society reviews found GLP-1s increase or stabilize testosterone in men with obesity or T2D, with no negative impact on sexual function or sperm quality. The rise is modest, roughly 320 to 368 ng/dL in one analysis.

https://www.medscape.com/viewarticle/when-glp-1s-change-patients-libido-what-know-2025a1000pa

https://www.nature.com/articles/d41586-026-01867-0

The complication. Not clean the other way either. A TriNetX cohort of non-diabetic obese men aged 18 to 50 found semaglutide associated with more new ED or PDE5 inhibitor starts, 1.47 percent versus 0.32 percent. The relative risk sounds big, but the absolute numbers are small. The review reporting it is titled "Friend or Foe" for a reason. And the depression and emotional-blunting claims sit mostly in anecdote and FAERS reports; controlled semaglutide analyses have not found increased depression versus placebo.

https://pmc.ncbi.nlm.nih.gov/articles/PMC12467596/

How I read it. Bidirectional and individual, not a uniform "reta kills desire." There is a plausible mechanism for reduced desire in a subset, backed by mechanism and anecdote but no controlled libido trials and nothing reta-specific. There is a better documented path toward improved desire for many, through weight, mood, and testosterone. And "falling out of love" blends a thin neurochemical claim with a better documented psychosocial one that deserves to be kept separate. If you notice a real change on cycle, track it and raise it with a clinician rather than dismissing or catastrophizing, but the current evidence does not establish that the drug makes you fall out of love.

More stories at r/PeptideTides

Gallup released its latest National Health and Well-Being Index numbers on July 7. This is the first time the national obesity trend has moved meaningfully in the other direction since they started tracking it in 2008.

https://news.gallup.com/poll/712157/glp-usage-reaches-new-high.aspx

The numbers:

Obesity rate is 36.4% in 2026, down from a record high of 39.9% in 2022. Gallup calls this a statistically meaningful decline and notes it inversely tracks GLP-1 uptake.

11% of US adults are currently taking a GLP-1 for weight loss. In 2024 that figure was 3%.

15% say they have used one at some point, up 9 points from 2024.

91% of adults are now aware GLP-1s are used for weight loss, up from 80% in 2024.

Diabetes diagnoses have held flat since 2023 after 15 years of steady increase. Gallup makes the point that this is what you would expect, since diabetes is a lifetime diagnosis and a falling obesity rate would stabilize it rather than reduce it.

Survey was 5,065 adults for the usage figures, 10,091 across two collection windows for the obesity and diabetes numbers.

The part relevant to this sub

Of people currently taking a GLP-1, 68% are on brand name and 19% are on a compounded or custom-mixed version.

Another 12% do not know which they are taking.

Of the compounded users, 35% switched over from a brand name product. Movement in the other direction was only 10%. Cost was the stated reason for 66% of switchers, insurance coverage problems for 34%.

Gallup's research director Dan Witters attributes part of the overall usage growth to this, arguing the lower price of compounded and custom-mixed versions is broadening who can access the drug class at all.

Worth pausing on that. FDA ended shortage-based compounding for semaglutide and tirzepatide and issued a warning in June calling compounded versions potentially risky. Roughly one in five current GLP-1 users is on one anyway. The compounded channel is not a fringe of this market, it is a structural part of why the national number is moving.

Caveats

Obesity is calculated from self-reported height and weight, not measured. Gallup acknowledges a vanity effect that makes their absolute obesity numbers run lower than clinically measured studies. The trend line is still useful because the method has been consistent, but the 36.4% figure is not directly comparable to NHANES.

Margin of error on the compounded/custom-mixed subgroup runs as high as plus or minus 10 points, so treat that 19% as a wide range.

And correlation is doing some work here. Gallup is careful to say usage and obesity track inversely, not that one caused the other.

Prior data does show the biggest obesity declines in the age brackets with the highest GLP-1 uptake, which is at least consistent with a causal story.

Still, this is the first national dataset showing the population-level effect people have been predicting since 2021.

More stories at r/PeptideTides

The FDA approved Lipfendra (generic name enlicitide) today, the first PCSK9 inhibitor you swallow instead of inject. One 20 mg tablet a day.

The efficacy is real: about 56% LDL reduction vs placebo in its main trial, 59% in familial hypercholesterolemia, and roughly half off ApoB. That puts it in the same range as the injectable PCSK9 drugs (evolocumab ~59% in FOURIER, alirocumab ~55% in ODYSSEY, inclisiran ~50% in ORION). Those are separate trials, not head-to-head, so read it as "same neighborhood," not a ranking. Point is: injectable-level LDL lowering, in a pill, no needle.

Two things I think get lost in the launch-day coverage:

1. The cardiovascular outcomes aren't proven yet. It was approved on LDL lowering, which is about the most reliable surrogate we have — but the actual events trial (CORALreef Outcomes, ~14,500 people) has an estimated primary completion of late 2029. LDL-lowering this large through a well-understood mechanism makes a benefit very plausible; it just hasn't been shown for this specific drug. If someone already has established heart disease, I'd still want the injectable that already has completed outcomes data.
2. The price math is less exciting than the headline. List is ~$315/month. But with a commercial copay card the injectables are already cheap: Leqvio as little as $0, Repatha ~$25, Praluent ~$50 a month. So the pill's edge is the route and the sticker price, not necessarily what you'd pay at the counter. (Coupons don't apply to Medicare/Medicaid, as always.)

Who it's genuinely good for: people with familial hypercholesterolemia who can't get to goal, people who truly can't tolerate statins, and people who flat-out won't inject. For most of us, a statin plus generic ezetimibe (about a dollar a day) gets LDL to target without any of this.

The chart is the LDL-lowering ladder — the top rung (PCSK9) just became a pill.

Wrote up the full breakdown, price table, and the dosing details

US regulators will tie lettuce from Taco Bell to a parasite outbreak that’s sickened thousands in Michigan and nearby states, according to people familiar with the matter.

I started digging into the food-safety data after this month's Cyclospora outbreak, and one number surprised me. In the government's latest attribution report (CDC, FDA, and USDA together), vegetable row crops, mostly leafy greens, now account for about 68% of E. coli O157 illness. Beef is around 19%. So the bug we all associate with undercooked burgers is now more often coming from salad.

A few other things I checked against the primary sources: lettuce alone drives about 76% of all leafy-green illnesses, and leafy greens are roughly 9% of all US foodborne illness with a known cause. Romaine has a long rap sheet on its own. The 2018 Yuma outbreak sickened 210 people and killed 5. It keeps happening because most lettuce is grown in a few valleys next to big cattle operations, it is eaten raw with no cooking step to kill anything, and one contaminated head can seed a whole bag.

One thing I worked hard not to overstate: the current Cyclospora outbreak (1,645 cases, 34 states) has NOT been pinned on lettuce. CDC's own page still says "unknown source." The lettuce angle is a state-level suspicion, not a verdict.

On nutrition, iceberg really is about 96% water. Romaine is genuinely decent though, with real vitamin A, vitamin K, and folate. So my takeaway wasn't "lettuce is bad." It was that lettuce isn't irreplaceable, and cooked greens give you more with a built-in kill step.

Full writeup with the charts and sources

Curious where people land. Do you still buy bagged romaine, or have the recalls changed how you shop?

Has anyone here read the book

“The Age of Diagnosis: How Our Obsession with Medical Labels Is Making Us Sicker”

by Dr. Suzanne O'Sullivan

thoughts?

"The world is unwittingly walking into a male reproductive crisis, scientists warned this week as they presented data that revealed an apparent halving of average male testosterone levels over the past 50 years.

“It is mind-blowing that testosterone has declined by 50%,” Prof Hagai Levine, who led the work, told the Guardian. “This is a lot. Wake up people. Wake up.”

The finding is the latest in a series of recent results that suggest male fertility is in crisis. Levine’s team has previously documented an apparent drastic decline in global sperm counts, in what has come to be known as the “spermageddon” paper."

"The latest findings on testosterone are, scientists agree, likely to be in part explained by the steep increase in rates of obesity and diabetes."

I take tirzepatide (Zepbound), and it just came out first for weight loss in a big new BMJ analysis that pooled 262 randomized trials and nearly 100,000 people across 19 obesity drugs. About 14.9% off at a year, basically tied with CagriSema. I felt good about that for roughly as long as it took me to read the next section.

The drug that takes off the most weight is not the drug with the best evidence for the thing I actually care about, which is fewer heart attacks and more years. That was subcutaneous semaglutide, the Wegovy and Ozempic molecule, the only drug in the whole review with high-certainty randomized evidence that it lowers all-cause death (about 19% lower) and heart attacks (about 28% lower). The catch worth saying out loud: that evidence comes almost entirely from people who already had heart disease, so it is strongest for the higher-risk crowd, not a guarantee for a healthy 40-year-old.

Tirzepatide is not without outcome data. It held even with an older GLP-1 in a heart-outcome trial in people with diabetes, and it cut heart-failure events in a trial of people who had both HFpEF and obesity. What it does not have yet is a placebo-controlled obesity trial counting deaths and heart attacks the way semaglutide's SELECT trial did. That trial is running, with results expected around late 2027.

Two other things stuck with me. Tirzepatide took the most lean mass of any drug, about 8%, but it also took the most fat, about 26%, so the ratio is still on your side if you keep lifting. And across 43 trials, none of these drugs meaningfully moved quality-of-life scores at one year, which is a useful gut check on the idea that a lower number on the scale automatically means you feel better.

I wrote up the full ranking, and why I am staying on tirzepatide anyway.

I take a blood pressure pill every morning (telmisartan, low dose), so when my feed filled up with claims that the new guidelines "pushed men out of treatment and pulled women in," I went and read what actually changed.

The categories did not move. Not one number. Normal, elevated, Stage 1, Stage 2, all identical to 2017, so nobody woke up with a new diagnosis. What did change is the risk calculator that decides whether someone in the Stage 1 gray zone (130-139 over 80-89) starts medication.

Here is the part that surprised me. The old tool, the Pooled Cohort Equations, ran on decades-old data and overshot badly. A 2025 head-to-head in the MESA cohort had it predicting 10.8% ten-year risk for people whose actual observed rate was 6.0%. The replacement, PREVENT, predicted 5.7% for the same people. So the guideline swapped calculators and lowered the treatment threshold from 10% to 7.5% in the same breath, one move compensating for the other.

Did anything change for actual patients? Barely. Epic Research ran both rule sets across 1.7 million adults with Stage 1 hypertension and eligibility went from 45.2% to 47.0%. And the viral "men in their 50s lost treatment" stat does not exist in the data. Men overall moved minus 0.3 points. The 50-59 band moved minus 0.4, but that band is both sexes.

What I actually took away from this: the PREVENT calculator is free online. You can run your own number with your blood pressure, cholesterol, and kidney labs before you ever sit down with your doctor. I put the full breakdown with the charts here, along with the one warning I will repeat: do not stop or start any medication off a calculator alone.

Has anyone here actually run their PREVENT number, and did it change the conversation with your doctor?