-Hello everyone.

Before we get going to the meat of this edition, let me go over a few issues.

First, I’m asked more often than I would expect, where the “Like” button is. Just a few days ago, someone wrote:

It depends upon where you read your version of The Arrow. If you read it via email, the button is as shown below:

If you read it online, it’s in a different spot.

I say at the bottom of each post to click the “Like” button if you enjoyed the post. I’m not all that tech oriented, but I see everyone else asking for Likes, so I did it, too. Although I have absolutely no idea how they might help me.

Next, a couple of mea culpas.

Last week I savaged the doctor who put in my stent for not writing a proper op report, so I could tell what really happened. He did write one and posted it, but it was after The Arrow had gone out.

As it turned out, it was a fairly complicated procedure to get the stent to go though the scarring at the junction of the right ureter and the bladder. Took him a long time to do it, but he got it done.

Also in the last Arrow I mentioned a doctor that I spoke with about the Natera/Signatera test. As you might recall, he told me that those kinds of tests aren’t all that accurate. I accused him of not knowing Jack. They are extremely accurate.

MD has a ritual every night before bed. She writes in one of those five-year diaries anything significant about the day’s activities. If she and I went somewhere or did something special on that same day the year before or the year before that, she reads it to me.

On the very day I sent out the last Arrow castigating the doc for not knowing Jack, she reads me her diary entry from the year before. Which is that on that very same day in 2025 — one year earlier — we visited the consulting oncologist in Oregon, who informed me of the Natera/Signatera test for the first time. I now know scads about them, but didn’t know Jack myself just one year earlier. So maybe he gets a reprieve.

But, in my defense, had someone asked me about the test a year and a week ago, I would have admitted that I didn’t know anything about it. Not some lame, half-mad bullshit about its not being very accurate.

Another reader asked

I did not take a specific glutamine blocker. But I did take pretty hefty doses of fenbendazole. It isn’t listed anywhere (that I could find, at least) as a glutamine inhibitor. But I did see a video of Thomas Seyfried saying that he was starting to use it as a glutamine inhibitor. I’ve been meaning to reach out to him about it, but I figured I would see him at a conference I attended a month or so ago, but he wasn’t there. I’ll see what I can find out.

Finally, I received the response below from a reader.

What he writes is absolutely true. The Signatera does provide greater resolution than a PET scan, but most docs aren’t aware of it. The thing that has surprised me the most out of this whole ordeal is that the rapid rise in my tumor burden after stopping the repurposed drugs is prima facia evidence that they were working. I’ve explained this to at least a half dozen doctors face to face, and with the sterling exception of our wonderful friend and my intrepid urologist in Louisiana, they don’t seem to grasp it at all. There is a huge lack of curiosity in the medical profession.

Okay, on to the main course…

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GLP-1ra vs GLP-1

I’m sure everyone reading these words knows about the existence of glucagon-like peptide 1 receptor agonists (which I’ll just call GLP-1ra). And I’m sure most sort of know how they work to bring about pretty hefty weight loss – primarily by reducing hunger.

No hunger means no eating, or not eating as much. And a reduced food intake generally leads to a reduction in weight.

But many people may not know that we make our own GLP-1. And that there are ways we can boost it a bit. And other ways we can quell hunger without the jabs.

Before we go on, let’s define what a GLP-1 receptor agonist is. GLP-1 is a type of hormone called an incretin. Hormones work by binding to a receptor. When they do bind to a particular receptor somewhere in the body, some sort of action is provoked. Drugs can bind to receptors and do two things. They can stimulate the receptors, or they can block or inhibit them. Those drugs that stimulate receptors are called agonists. As we’ll discuss shortly, your own GLP-1, the one your body makes, binds to a GLP-1 receptor and generates a downstream action. GLP-1 receptor agonists drugs do the same thing. They bind to the GLP-1 receptors and stimulate them. So for purposes of this essay, which will be about both GLP-1 and GLP-1 receptor agonists, I’ll refer to the GLP-1 your body makes as GLP-1. And the drug as GLP-1ra.

It would be an understatement to say that these drugs have been anything but blockbusters in terms of pharmaceutical profits. Of course, the pharmaceutical industry wants the sales to go on and on and on. And the cash registers to go ching, ching, ching. And hooking it to as many benefits as possible ensures that. Since obesity is known as a risk factor for countless other issues – cancer, diabetes, heart disease, osteoarthritis, sleep apnea, hypertension, fatty liver, GERD, and reduced life expectancy, just to name the ones that immediately jump to mind – any medication that brings about weight loss could reasonably be touted to cure or at least mitigate one or more of these issues.

Thus all the press reports popping up almost every day about how these drugs are being studied as preventative for one or more of the issues mentioned above. It makes sense from a financial perspective. Insurance companies and even Medicare are loath to pay for expensive drugs for a condition – obesity – that most people believe to be self induced. (Though they never had trouble paying for treatment of smoking-related lung cancer, but I digress.)

And then there is the problem of weight regain. Go off the meds, then all the weight comes back. That, sadly, is the case for virtually all obesity treatments. When the treatment ends, the weight returns. An astounding fact is that obesity has a worse long-term prognosis than cancer.

But that’s not really what I want to talk about here.

I want to discuss how these drugs actually work. And how you can harness your own GLP-1 and other incretins (the broad category name for these kinds of hormones) to work for you.

The first of the two main types of incretins so far identified are glucose-dependent insulinotropic polypeptide, which used to be called gastric inhibitory polypeptide, thus the initials GIP, as it is still referred to these days. And the second, glucagon-like peptide-1, called GLP-1, which is the more familiar one.

The first of the new weight-loss drugs were basically those acting to increase GLP-1. A second tier came along and added GIP to the GLP-1 action. And now there is one that contains a GLP-1ra, a GIPra, and the hormone glucagon. Each addition to the pile seems to increase the amount of weight their study subjects lost. And, to be mercenary about it, each new addition means it is a new drug and that gives the pharmaceutical company that developed it a few years longer to charge sky high prices before it goes off patent.

The first incretin was discovered in the mid-1960s by researchers at the University of Colorado. They gave subjects a dose of glucose much like a glucose tolerance test and measured their insulin response. They then gave glucose to the same subjects intravenously and discovered they had only a small increase in insulin levels as compared to when they gave the glucose orally. From this markedly different insulin response, they realized that there must be some sort of surveillance cells in the GI tract that sense the glucose (and carbs in general) coming down the pipe and signal to the pancreas to release insulin before the carbs are actually absorbed and make it into the blood stream.

As it turned out, a couple of these surveillance cells were identified to be L cells and K cells that are located in various parts of the GI tract. These cells release a sort of hormone (an incretin) that travels to the pancreas and other cells to help regulate the response of insulin and glucagon. The incretins these cells release are GIP and GLP-1.

Until these latest weight loss drugs came along, very few people knew what incretins were. I gave a talk on incretins in Denver about seven years or so ago. Before I started, I asked for a show of hands from anyone who knew what an incretin was. Just a few hands went up out of a pretty large audience. I suspect that if I gave this talk today, most every hand would go up.

Here are a couple of slides from that presentation showing what is called the incretin effect, i.e, the much larger increase in insulin secretion following an oral load (PO, standing for per os, by mouth) of glucose versus an IV load.

As you can see from the images above, incretins drive a significant increase in insulin levels. (The incretin response is represented by the red vertical lines.) At the same time they end up decreasing glucagon levels. Since insulin drives fat storage and glucagon does just the opposite, how in the heck do GLP-1ra drugs that do these very things bring about weight loss?

It would seem they would do the exact opposite.

If you lower your insulin levels, the fat cells release their contents (stored fat) to burn as fuel. Glucagon helps the process along. It would seem, based on their actions, that GLP-1ra drugs would make those who take them gain weight, not lose it. But they don’t.

GLP-1 has another effect along with raising insulin and lowering glucagon – it also decreases gastric motility. Which means your stomach empties more slowly, bringing about a decrease in hunger. And these incretin-based drugs also probably affect other hunger centers in the brain, because they really squelch hunger in most of those who take them.

As it turns out, the hunger suppressing mechanism of these drugs overrides the increased insulin and decreased glucagon they bring about.

If this is how it all works, why doesn’t our own GLP-1 have these same effects?

Mainly because of a protein called dipeptidyl peptidase-4, which we will refer to as DPP-4.

When we eat, and we initiate the incretin effect – insulin up and glucagon down – the incretins hang around for only a few minutes at best. DPP-4 is released, and it basically destroys the GLP-1. Thanks to the rapid response of DPP-4, your native GLP-1 has a half life in the body of just a few minutes.

Since diabetes is such a vast and growing market for drugs to treat it, the pharmaceutical companies have been fiddling with incretins for years, mainly as a means to keep blood glucose under control. Incretins increase insulin and decrease glucagon, both of which will work to keep glucose down, but too much insulin and not enough glucagon is the very problem the obese suffer from. So it seems strange that these incretin hormones would help people who already have high insulin and low glucagon lose weight. It’s paradoxical.

But these hormones, especially GLP-1, have another powerful effect. They reduce gastric motility – the speed at which food passes through the gut – which significantly reduces hunger. The potent reduction in hunger overrides the increase in insulin and fall in glucagon.

It would seem like a simple task for pharmaceutical scientists to fiddle around with incretins such as GLP-1 to make them longer acting. And though it took a while, they were ultimately successful. By taking the backbone of the structure of GLP-1 and replacing a few proteins here and there, scientists created the first GLP-1 drug for diabetes.¹

The drug, called liraglutide and sold under the name Saxenda, was approved by the FDA for use in 2010. The drug was administered via a daily injection. Drug chemists had figured out how to increase the duration of action from a few minutes to an entire day by preventing its immediate breakdown by DPP-4 prolonging hunger reduction.

Those using Saxenda lost weight, which spurred the drug companies to ever more fevered research on these drugs as weight-loss medications. They came up with Ozempic, which was approved in late 2017. It required only a weekly injection, which was much more palatable to the masses than a daily injection. Although Ozempic was approved by the FDA as a treatment for diabetes, it started the trend for off-label use as a weight-loss drug and the flood gates opened.

Then came Wegovy – the same drug as Ozempic – but at a higher dose. It was approved by the FDA for weight management in 2021. And the race was on to come up with bigger and better incretin-based drugs, which is where we find ourselves now.

Let me back up for a bit.

In 2006 the first DPP-4 inhibitors hit the market. These drugs inhibit or inactivate the enzyme DPP-4 that inactivates GLP-1 and GIP. Since both GLP-1 and GIP increase the release of insulin from the pancreas, it would seem to make sense to inhibit the enzyme that inactivated both of them. And it did. DPP-4 inhibitors resulted in an increase in insulin secretion, producing a modest glucose lowering without the risk of hypoglycemia. They were pretty much weight neutral, so not a lot of effort was spent trying to develop them as weight-loss drugs.

Below is a short explainer video on how DPP-4 works.

As I mentioned above, an increase in insulin levels coupled with a decrease in glucagon levels is a set up for weight gain. The GLP-1ra drugs bring about this very hormonal result – higher insulin and lower glucagon – yet they without question bring about significant weight loss.

What gives?

In the video above, it shows the three things I already mentioned that these drugs do: they increase insulin, decrease glucagon, and reduce hunger. 

And, again, since these drugs work as well as they do, the reduction in hunger vastly overrides the fat storage effects of increased insulin and decreased glucagon. In some measure because there’s not much coming in to store.

So, how can we get the GLP-1 response without getting the shots? And without increasing insulin levels?

A number of researchers have studied this very issue.

There are three foods that will increase GLP-1. These are, in order of effectiveness, protein, fat, and fiber.

Protein stimulates the release of GLP-1 in a dose-related manner. The more you eat, the more GLP-1 you release. But you need to start with at least 25 grams to kick it off. From there on, the more you eat, the more GLP-1 you will produce.

The second food running a close second to protein is fat. The papers I read all said monounsaturated fat (MUFA) generated the most GLP-1 response, but I’m always skeptical of those kinds of papers. Many researchers fear that if they in any way promote saturated fat (SFA), they won’t get published. It’s always safe therefore to go with MUFA, which they almost always do.

But in this case, it’s no biggie because red meat has as much MUFA as it does SFA. The fatty acid composition of a typical beef steak is 45-50% SFA, 45-50% MUFA, and 4-7% of PUFA. The same pretty much goes for lamb, which clocks in at 40-50% SFA, 35–45% MUFA, and 5–10% PUFA.

Pork fat is ~48% SFA, ~37% MUFA, and ~15% PUFA. So a little more PUFA and little less MUFA in our porky friends, but not that much difference to worry about.

Chicken fat, surprisingly, is ~30–45% SFU, ~35–50% MUFA, and ~15–30% PUFA. A bit more PUFA than the others, but still plenty of SFA and MUFA. If you get your protein from meat, you’re going to get a bump in GLP-1 and a reduction in hunger.

The nice thing about protein is that although it does raise insulin a bit, it also raises glucagon to go along with it. If you’re looking for weight loss, glucagon is good, insulin is bad.

Most of the studies I looked at to see what raises native GLP-1 included fiber after protein and fat. As with the monounsaturated fat, I’m not sure I entirely buy into the notion that fiber does much of anything. It’s the academically correct thing to say, though, but whether it does anything or not to significantly raise GLP-1, I tend to question.

I’ll give fiber the benefit of the doubt, however, as virtually all of the fruits and vegetables that are a part of a whole-food, low-carb diet contain a fair amount of fiber.

Another thing you can do to raise your GLP-1 is to inhibit your DPP-4. Which is a tougher task. DPP-4 is more active in subjects who are obese and who have insulin resistance. As you lose weight, you will decrease the activity of your DPP-4, and will consequently keep your own GLP-1 around longer. And be less hungry.

I found one paper from a couple of independent researchers describing a number of supplements that can inhibit DPP-4. The researchers are both part of a company, so I suspect they’re testing a product to sell. That doesn’t make the product bad or unworthy, but it isn’t an arm’s length, randomized controlled study. I couldn’t find the actual supplement for sale anywhere, but you can see from the chart below the many components it contains and how they all inhibit DPP-4.

If anyone has any experience with these supplements, I would be keenly interested in hearing about it.

There are a couple of other substances your body produces that are GLP-1-like, not in their structure, but in their ability to decrease hunger. As I discussed above, the main effect of the GLP-1ra drugs is not something magic. It’s simply a potent reduction in appetite.

Now, you’ll never be able to get your own GLP-1 to stick around for a week like the drugs do. What I’m doing here, though, is provide the info on how you can manipulate your own endogenous enzymes and hormones to reduce hunger. And prevent you from thinking about food all the time. Which is, I suppose, what they are now calling ‘quieting food noise’.

One of the other peptides you produce along with GLP-1 is called peptide YY. PYY is released by the same foods that increase GLP-1 and at the same time. Protein and fat. PYY acts when the nutrients reach the lower part of the small intestine. PYY along with another peptide we’ll discuss next, activates what is called the ileal brake. (The ileum is the lower end of the small intestine.)

The ileal brake does as its name implies – it decreases the activity of the lower end of the gut. This decrease in activity ends up slowing the transit of food, and typically feeds back to the brain and reduces appetite. Unfortunately, PYY is blunted to a degree by obesity and insulin resistance. I know, it just isn’t fair.

Another peptide that also more or less activates the ileal brake is cholecystokinin (CCK). CCK responds primarily to fat coming down the upper portion of the GI tract. It also sends a message to the brain that we are fully fed, so shut off the hunger.

One of the ways you can co-opt these two peptides to your own benefit is to eat a fatty snack 30 to 40 minutes before you eat your largest meal of the day. Macadamia nuts, which are simply little balls of fat with a bit of protein thrown in are ideal. Eat a small handful a bit before, and it will significantly blunt your hunger via the ileal brake before you sit down to dine.

There are two other foods that have a nice appetite suppressing effect. One is whey protein; the other is casein, another milk protein. They are both dairy proteins, but have different actions.

Whey tends to have a fairly rapid effect in terms of blunting appetite, while casein kicks in a bit later. Since cream contains a fair amount of casein, you can mix it with whey protein and make a shake that will reduce appetite quickly and last over the longer term.

If you do try the shake route, I would recommend you get A2 cream or half and half, which comes mainly from jersey cows and will be labeled A2/A2 on the carton. The GI tract breaks the A1 casein down into a substance that causes some people to have bloating, constipation, and other GI issues. That usually isn’t the case with A2 casein. If you use goat’s milk, or sheep or buffalo milk, they don’t contain A1 casein, only A2. Either one works okay to inhibit appetite, but some people do better as far as GI symptoms go with A2. And, it’s probably all in my head, but I like the taste of A2 better.

If I drink a whey protein/cream shake in the middle of the morning, I don’t even think about food until late in the afternoon. Your mileage may vary.

Another phenomenon researchers have discovered about eating is that soft foods encourage more eating than do harder foods. One study showed that subjects consuming both ultraprocessed foods or minimally processed foods that are soft consumed ~360 more kcals than when eating harder to chew foods that were ultraprocessed or minimally processed.

A number of rationales were offered as a reason why this should be. My own take on it is that people consume soft foods more rapidly than hard foods. Slower eating provides more time for the nutrients to head down the gut and trigger the ileal brake.

One of the studies I explained in my talk linked above was a mouse study, but it graphically demonstrates what happens.

Researchers fed mice one of three diets: A high-fat diet, a so-called Western high-fat diet (a diet composed of what people today might find in a cafeteria), and a rodent chow diet. As you can see from the graphic below, the mice gained the greatest amount of weight on the high-fat diet, followed by the Western diet, whereas those on chow gained the least.

The first two diets were much softer – the high-fat diet the softest of all – while the chow diets were hard pellets. When the researchers repeated the experiment with the diets modified to be the same consistency, there was no difference in weight gain.

Granted, these were rodent studies, but, based on other human studies that can’t be this well controlled, I strongly suspect the same effect applies to us.

If we favor foods that take a bit of time to chew, we eat less. But the food is still filling, because the ileal brake kicks in and slows the transit through the GI tract and diminishes hunger.

Although we’ll never be able to make our own GLP-1 work as well as the GLP-1ra drugs, there are many steps we can take to ward off hunger. Which is the main effect of GLP-1ra drugs. And we can do it without taking expensive drugs, with a bevy of side effects, and the long-term ones of which may yet be discovered. I lived through the phen-fen debacle years ago. At that time, phen-fen was treated as being the same miracle for weight loss as the GLP-1ra drugs are now. Everybody was clamoring for them.

Then all the lawsuits hit. MD and I had a few patients who took them, but mostly we tried to talk our own patients off the ledge and worked with them to help them stay on their low-carb diets.

I’ve got to admit, though, that I did break from my refusal to give scripts for phen-fen. A now ex-in-law hounded me relentlessly for a prescription. I finally succumbed and gave her one. Sure enough, several years later, I get a letter from a lawyer wanting her medical records. She was claiming an issue with the phen-fen I prescribed for her years before and was wanting to get in on the settlement money from the drug company.

No good deed ever goes unpunished.

One caveat to all the above about the ways to significantly reduce hunger. It can all be blown with the wrong dessert.

The fat-sugar combo is difficult to resist, which is why almost all sweets are some mix of sugar and fat. I’ll remind you of the bite of swordfish analogy I’ve used before. Imagine that you’ve just had a wonderful dinner of a big steak, a salad, and some steamed asparagus. It was a really big steak, so you are full as a tick. One of your dinner companions asks you to give his/her swordfish a try. “It’s so delicious.” But you say, no, no, I couldn’t eat another bite.

We’ve all been there. All our hunger-suppressing hormones are doing their jobs.

Then comes the dessert tray.

We’ve all been there, too.

Even though we were too stuffed to try the swordfish, we weren't too stuffed to go facedown in some gooey dessert that has three times the volume and calories of the swordfish. Refined carbs will override all of our hunger suppression.

Always bear this in mind. If you must have dessert, go for a fruit and cheese plate, or something similar. If you follow the outline I laid out above to prevent hunger, just beware of dessert.

If you stick with protein and fat, with a little fiber thrown in from low-carb fruits and vegetables, you’ll give your own GLP-1 a chance to work better. Combining this with some whey and casein, while avoiding soft (or liquid) foods, will do everything you can do (short of taking drugs) to reduce hunger, while still consuming a more than adequate diet. Plus, you won’t experience any of the long list of side effects of the GLP-1ra meds that are being reported on nearly every day.

1. The first GLP-1–based diabetes drug was exenatide, marketed as Byetta. Approved in 2005, Exenatide is a synthetic version of a peptide originally identified in Gila monster venom. It activates the GLP-1 receptor but is not identical to native human GLP-1.

Odds and Ends

• The deepest I ever SCUBA dived in the ocean was maybe 120 feet, never deep enough, long enough to have to decompress. So most of these bizarre and curious deep sea creatures I've never seen close up and in 'person'. 

• The Bride and I (especially the Bride) have bemoaned the loss of color in neighborhoods. Home after home on block after block newly painted white with black trim or gray trim. Every interior black and white and 50 shades of gray. So stark on the outside and dull on the inside. And we're not the only ones who have noticed as this interesting Atlantic article makes clear.

• What's believed to be the world's first motor hotel (motel) has gone up for sale. It's been closed since 1991, apparently, but  probably just needs a good cleaning and a coat of paint. Not that I'm interested in buying, but it was a trip looking back on the old California past.

• MD when confronted once in a live radio interview by a vegan who bemoaned our advocating meat eating as inflicting fear, pain, and/or death on innocent animals countered that she (the vegan) was engaging in species chauvinism. 'Just because you can't hear the carrots scream when you pull them out by their roots doesn't mean they don't.'  Looks like there might be a grain of truth to their screaming, at least as it pertains to cauliflower and rhubarb. 

• Fascinating facts about The King (and no, I don’t mean Charles III), one of my all time favorite musical artists. Some I knew; some I didn't.

• Do as the Romans do. Good advice for construction to be sure. And a new start up has proven that everything old is new again. Including a Roman formula for longer lasting, self-healing concrete.

• You can see Thomas Edison's last breath. Or at least a tube said to contain air from near his bedside when he died and sealed upon his death. It's on display at the amazing Henry Ford Museum in Dearborn, MI, which if you haven't visited is well worth the trip. MD and I have been several times (having family in Michigan) at various seasons of the year. The run-up to Christmas is especially magical. Highly recommend it.

• Catnip for doom scrollers. An interactive map of all the wildfires, floods, and other natural disasters going on in the US. Personally, I'm spending too much time already on watching the shipping traffic in the Strait of Hormuz.

• 'Latin's a dead language, as dead as it can be. First it killed the Romans and now it's killing me.' Every student of the language likely recited that little ditty to protest having to learn conjugations and declensions, but is the language really dead? No, it isn't. It lives on in an office of the Vatican, including adding new Latin words like 'helocopterum' for the whirlybird the ancient Romans never saw. And more...

• Interesting historical bit about what George Washington typically ate every day. He wasn't as big a meat eater as most of his contemporaries, tending toward softer foods and liquids, largely because his notoriously bad teeth made it hard to chew it.

• Americans are apparently drinking less, according to a new report on whisky sales. Research puts it down to GenZ's lack of interest in alcohol. MD is convinced, now that the epic Outlander series has aired its finale, it is the loss of the Outlander effect, since it's almost impossible to watch it and not feel the urge to sip on a dram of whisky. 

• MD and I once on a cruise in Alaska kayaked upstream from the sea to see the salmon spawning, and it was amazing. Hundreds of them were jumping all around us to the point we thought one would likely land in our laps. It's the only one of these 6 great US animal migrations we've ever witnessed, but we're game to see others.

• Here's a look at the evolution of school lunches over the last century. At 79, I lived through a good bit of it. MD, too. We remember in the 50s and 60s having divided trays with some kind of meat (sometimes what we loving called mystery meat), some kind of starch (corn kernels or potatoes usually, but occasionally mac'n'cheese), some kind of vegetable, usually green beans or green peas, a big yeast roll and maybe a fruit (apple usually) or small serving of dessert, such as chocolate pudding or apple cobbler, or the perennial favorite, cinnamon rolls. And whole milk -- chocolate or white. And on Fridays, a clean-out-the-walk-in-fridge vegetable soup of leftovers of whatever we'd had all week. How does this list comport with your recollections?

Newsletter Recommendations

Video of the Week

Well, this VOTW should have been expected. I love Dolly Parton. I grew up watching here. Like me, she is of Borderer stock. I can’t even hold her flacking for the mRNA jabs against her. They may have hastened her death from what appeared to be a pretty rapidly advancing cancer. She had one of the most naturally beautiful voices around, and she absolutely made the best of it. Of all the songs she wrote, here is my favorite.

RIP

Time for the poll, so you can grade my performance this week.

That’s about it for this week. Keep in good cheer, and I’ll be back soon.

Please help me out by clicking the Like button, assuming, of course, that you like it.

This newsletter is for informational and educational purposes only. It is not, nor is it intended to be, a substitute for professional medical advice, diagnosis, or treatment and should never be relied upon for specific medical advice.

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