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Elite Medical Care, 541 Wiley Parker Road, Jackson, TN (2026)

10/24/2026

Voting is both a civic duty and an act of hope. 🇺🇸

I understand the cynicism. Sometimes it feels as though our votes don’t matter, that money, lobbying, political interests, and powerful institutions have more influence over our future than ordinary citizens ever will. And while we call ourselves a democracy, we are technically a constitutional republic with democratic elections—not a system of direct democracy where the people always get the final say.

But if we surrender our voices because we believe the system is broken, we guarantee that others will make our decisions for us.

Vote—not because the system is perfect, but because giving up is exactly what allows it to remain imperfect. Question the system, demand accountability, and never confuse cynicism with powerlessness. Our democracy is only as strong as our willingness to participate and our courage to demand better.

10/20/2026

I am Dr. Brad, and here's what you need to know about regurgitation. 🩺

**Clinical Renal Physiology: Understanding Vomiting-Induced Metabolic Alkalosis**

**Question: Why does vomiting cause metabolic alkalosis with aciduria?**

Let's break down the physiology.

When we vomit, we lose hydrochloric acid (HCl), which means we're losing both hydrogen ions (H⁺) and chloride (Cl⁻). Losing hydrogen ions increases serum bicarbonate relative to hydrogen ions, producing **metabolic alkalosis**. The associated chloride loss and fluid depletion make it even harder for the kidneys to correct the problem.

Here's where the physiology gets interesting.

**1. Volume depletion activates the renin-angiotensin-aldosterone system (RAAS).**

As fluid volume decreases, the kidneys activate RAAS, ultimately increasing aldosterone secretion. Aldosterone promotes sodium reabsorption while increasing potassium and hydrogen ion secretion in the distal nephron.

The result? The kidneys continue excreting hydrogen ions, which can produce **acidic urine despite systemic metabolic alkalosis**. This is called *paradoxical aciduria*.

**2. Why is chloride so important?**

Remember the chloride-bicarbonate exchange mechanism in the kidney? Chloride availability is essential for bicarbonate secretion through the pendrin exchanger in the collecting duct's beta-intercalated cells.

When chloride is depleted, the kidney's ability to excrete bicarbonate is impaired. Bicarbonate remains in the bloodstream, perpetuating the metabolic alkalosis.

**3. What's the treatment?**

For a patient with chloride-responsive metabolic alkalosis and volume depletion, **isotonic saline (0.9% sodium chloride)** can help correct the underlying problem.

The sodium and chloride restore extracellular fluid volume and chloride availability, helping the kidneys excrete excess bicarbonate. As volume depletion resolves, RAAS activation decreases, allowing the kidneys to correct the alkalosis more effectively.

Potassium deficits should also be assessed and corrected when indicated.

🧠 **The takeaway:**

Vomiting → H⁺ and Cl⁻ loss → metabolic alkalosis + volume depletion → RAAS activation → increased renal H⁺ secretion → paradoxical aciduria.

**Remember:** The blood is alkalotic, but the urine can be acidic. And chloride is a key part of correcting the problem.

That's the physiology behind the question of the day. Know the mechanism, and the treatment makes sense.

10/10/2026

**Hello, I’m Dr. Brad, and here’s what you need to know about retatrutide.**

As the science of obesity medicine continues to evolve, understanding the mechanisms behind these emerging therapies is becoming increasingly important. Patients deserve healthcare providers who stay informed, understand the evidence, and can translate advances in metabolic medicine into thoughtful, evidence-based treatment decisions.

**Retatrutide: Are We Entering a New Era of Obesity Medicine?**

Eli Lilly’s investigational triple-hormone receptor agonist, retatrutide, is generating considerable excitement in metabolic medicine—and for good reason. Its unique approach to weight management represents a potentially important evolution in how we treat obesity and its associated metabolic complications.

At the highest studied dose of 12 mg, retatrutide has demonstrated remarkable weight-loss potential in clinical trials. Results in adults without type 2 diabetes have approached the 25–30% range of initial body weight over extended treatment periods. Significant weight loss has also been observed in adults with type 2 diabetes, a population that generally experiences less weight reduction with incretin-based therapies.

Why does this matter? Obesity and type 2 diabetes are closely interconnected, and metabolic factors—including insulin resistance—can influence treatment response. Achieving substantial weight reduction in patients with diabetes remains an important objective in the development of next-generation obesity therapies.

**So, what makes retatrutide different?**

The answer lies in its mechanism of action. Retatrutide targets three distinct hormone receptors simultaneously:

**1. GLP-1 — Glucagon-like peptide-1**

Semaglutide, marketed as Ozempic and Wegovy, activates the GLP-1 receptor. This pathway helps regulate appetite, food intake, and glucose homeostasis.

**2. GIP — Glucose-dependent insulinotropic polypeptide**

Tirzepatide, marketed as Mounjaro and Zepbound, activates both the GIP and GLP-1 receptors. These complementary pathways influence glucose regulation, insulin secretion, and metabolic function.

**3. Glucagon**

This is the additional component that makes retatrutide particularly intriguing. Glucagon receptor activation may increase energy expenditure and influence how the body mobilizes and utilizes stored energy.

Here is the key concept: retatrutide may influence weight management from two complementary directions. It helps reduce energy intake through effects on appetite and satiety while potentially increasing energy expenditure through glucagon receptor activity.

In simpler terms, the therapeutic strategy is to help the body take in less energy while potentially using more of it. Rather than targeting appetite and glucose regulation alone, retatrutide is designed to influence several interconnected metabolic pathways involved in energy balance.

This triple-receptor approach may help explain the substantial weight reductions observed during clinical development. However, the precise contribution of each receptor pathway remains under investigation, and direct head-to-head trials are necessary to establish how retatrutide compares with existing medications.

**What comes next?**

The next major milestones include comparative efficacy studies, long-term safety assessments, and cardiovascular outcomes research. These findings will help determine retatrutide’s eventual role in treating obesity, type 2 diabetes, and related metabolic conditions.

Given the enormous unmet need in obesity medicine, I am optimistic about the potential of this investigational therapy. If its efficacy and safety are confirmed, retatrutide could become an important addition to our treatment options.

It is important to remember that retatrutide remains investigational and is not FDA-approved. Its long-term safety profile and overall clinical role must be established through appropriate clinical trials and regulatory review.

**My perspective as a clinical pharmacist specializing in family medicine:** The future of obesity treatment may involve more than targeting a single hormone pathway. By addressing multiple metabolic mechanisms simultaneously, we may be moving toward a more comprehensive approach to managing obesity and its associated diseases.

Understanding a medication means looking beyond its brand name. It means understanding its pharmacology, clinical evidence, limitations, safety profile, and appropriate place in therapy.

As obesity medicine continues to advance, patients and providers alike should remain curious, informed, and committed to evidence-based care.

**The future of obesity treatment may not be about targeting one pathway. It may be about understanding how multiple pathways work together to produce meaningful metabolic change.**

— **Dr. Brad Medling, Pharm.D.**\
Clinical Pharmacist Practitioner | Family Medicine

10/02/2026

RETATRUTIDE: WHEN METABOLIC PHARMACOLOGY BECOMES MORE THAN WEIGHT LOSS

There is a tendency to describe the newest generation of incretin therapies simply as “weight-loss drugs.” That characterization is increasingly inadequate.

The emerging data surrounding retatrutide suggest that we may be witnessing something considerably more sophisticated: the deliberate manipulation of multiple physiologic pathways governing appetite, glucose homeostasis, hepatic metabolism, lipid utilization, and energy expenditure.

The distinction is important.

Patients with obesity and type 2 diabetes represent one of the most metabolically complex populations in obesity medicine. Insulin resistance, hyperinsulinemia, impaired metabolic flexibility, ectopic lipid accumulation, and dysregulated appetite signaling create a physiologic environment in which meaningful and sustained weight reduction can be difficult to achieve.

Retatrutide approaches this problem differently.

Rather than targeting a single hormonal pathway, it simultaneously activates GLP-1, GIP, and glucagon receptors.

GLP-1 contributes to appetite regulation, satiety, delayed gastric emptying, and glucose-dependent insulin secretion. GIP provides complementary incretin and metabolic effects. Glucagon introduces an additional dimension: increased hepatic energy mobilization, stimulation of lipid utilization, and effects on energy expenditure.

That third pathway is particularly fascinating.

The objective is not merely to suppress appetite. The pharmacologic concept is to alter the body's energy balance and substrate utilization at multiple physiologic levels simultaneously.

And the magnitude of the reported clinical effect is difficult to ignore.

In the TRIUMPH-2 population, participants receiving the highest studied dose achieved approximately 21% mean body-weight reduction over 80 weeks, with the highest-baseline-BMI subgroup exceeding 23% average weight loss.

Those numbers represent substantially more than cosmetic weight reduction.

They potentially represent a clinically meaningful alteration in the metabolic phenotype of patients with obesity and type 2 diabetes.

The improvements were not limited to body weight. The study reported substantial reductions in HbA1c, triglycerides, and waist circumference, with a significant proportion of participants achieving an HbA1c below 5.7%.

This is where the discussion becomes considerably more interesting.

If pharmacologic therapy can simultaneously reduce adiposity, improve glycemic regulation, decrease visceral adiposity, improve lipid parameters, and potentially alter hepatic energy metabolism, then we are no longer talking about a medication that merely makes a patient eat less.

We are talking about metabolic pharmacology.

That distinction may ultimately prove to be one of the most important developments in modern obesity medicine.

However, scientific enthusiasm should never outrun the evidence.

Retatrutide remains investigational and is not FDA-approved. Its eventual role in clinical practice will depend upon continued evaluation of long-term safety, cardiovascular and other clinical outcomes, durability of weight reduction, tolerability, and comparative effectiveness against currently approved therapies.

There is also an increasingly important public-health issue surrounding unapproved and purportedly compounded versions of investigational medications. A molecule demonstrated in a controlled clinical trial should not automatically be equated with a product being marketed through social media or obtained from an unverified source.

The molecule, the clinical trial, the manufactured product, and the regulatory status are four separate questions.

For clinicians, that distinction matters.

What fascinates me most about retatrutide is not simply that patients may lose 20% or more of their body weight.

It is that we are beginning to understand obesity less as a failure of willpower and more as a complex, biologically regulated disease involving multiple interacting hormonal and metabolic systems.

And perhaps the next generation of therapy will not be defined by finding a stronger appetite suppressant.

Perhaps it will be defined by learning how to re-engineer the metabolic physiology of obesity itself.

Dr. Brad Medling, Pharm.D.
Clinical Pharmacist Practitioner | Family Medicine

09/17/2026

Have you ever wondered why your blood sugar is elevated when you wake up, even though you haven't eaten anything?

I'm Dr. Brad. Let's talk about something called the dawn phenomenon.

You may notice that your blood glucose is relatively well controlled throughout the day, but when you wake up in the morning, your fasting blood sugar is unexpectedly elevated.

So, what's happening?

As your body prepares to wake up, it releases hormones such as cortisol, growth hormone, and glucagon. These hormones signal your liver to increase glucose production and release stored glucose into your bloodstream.

Your liver does this through processes called gluconeogenesis and glycogenolysis.

Essentially, your body is preparing to wake up and needs energy. Your liver responds by making glucose available to fuel your body's activities.

This natural increase in blood glucose in the early morning hours is known as the dawn phenomenon.

Now, an occasional elevation may not be concerning. However, if your fasting glucose is consistently elevated, it's important to investigate what's happening.

Your medication regimen, overnight glucose patterns, diet, and other factors may need to be evaluated.

Don't adjust your medications or insulin based on one elevated reading without guidance from your healthcare provider. Follow the individualized treatment plan your provider has established for you.

If you're experiencing consistently elevated fasting glucose and haven't received guidance on how to manage it, reach out to your healthcare provider.

And if you need assistance with diabetes management, you can message me at Elite Medical Care to inquire about consultation availability, insurance information, and pricing.

I hope this helps you better understand your blood sugar and what's happening inside your body.

Take care, and remember: understanding your numbers is an important part of managing your health.

09/08/2026

Everyone listen up! I've just been told the craziest thing. They're making a day to where things can get better. They're calling it, Tomorrow. Saiko!

09/06/2026

I'm Dr. Medling of Elite Medical Care. One area where my background in chemistry and pharmacology has been particularly valuable clinically is understanding fluid resuscitation.

When I think about IV fluids, I use a fairly simple framework:

Is this a resuscitation fluid, or is this a maintenance fluid?

💧 RESUSCITATION FLUIDS

When a patient is volume depleted, hypotensive, or actively hemorrhaging, the goal is intravascular volume replacement and restoration of perfusion.

The primary crystalloid options are:

• 0.9% Sodium Chloride (Normal Saline)
• Lactated Ringer's

Normal saline contains approximately 154 mEq/L of sodium and 154 mEq/L of chloride, producing an osmolarity of approximately 308 mOsm/L.

That makes it an effective isotonic crystalloid for volume resuscitation.

However, there is an important physiologic caveat: giving large volumes of normal saline can produce hyperchloremic metabolic acidosis. This is one reason balanced crystalloids such as Lactated Ringer's are frequently favored when clinically appropriate.

And then there is blood.

If a patient is hemorrhaging, remember:

They aren't bleeding normal saline.
They aren't bleeding packed RBCs.
They aren't bleeding FFP.
They aren't bleeding platelets.

They're bleeding whole blood.

That is why whole blood is an incredibly valuable resuscitative product in the appropriate trauma/hemorrhage setting.

When whole blood isn't being used, we can utilize component therapy through a Massive Transfusion Protocol (MTP).

Traditionally, this involves balanced administration of:

1 unit PRBC : 1 unit FFP : 1 platelet dose

The objective is to replace not only red blood cells, but also the coagulation factors and platelets being lost during massive hemorrhage.

And how do we determine what the patient actually needs?

Traditional coagulation studies include:

• PT
• PTT
• INR

But increasingly, we can use viscoelastic testing such as TEG (thromboelastography) to evaluate the patient's actual clot formation and breakdown in real time.

TEG essentially gives us a functional picture of the coagulation process and can help guide targeted blood-product replacement rather than simply treating laboratory numbers in isolation.

💧 MAINTENANCE FLUIDS

Now completely different scenario:

A patient has a bowel obstruction, is NPO, has an NG tube to suction, and has been losing significant GI fluid for several days.

That's where I start thinking about maintenance requirements and ongoing electrolyte losses, rather than simply "giving fluids."

Electrolytes matter.

In these patients, monitoring a BMP along with magnesium and phosphorus can be extremely important, particularly when there is prolonged GI decompression or significant ongoing losses.

The classic maintenance fluid many of us learned is:

D5 ½ NS + 20 mEq KCl

Of course, the actual fluid choice should be individualized based on the patient's clinical status, renal function, serum electrolytes, glucose, acid-base status, and ongoing losses.

And how much?

For pediatrics, the classic calculation is the 4-2-1 rule for hourly maintenance fluids.

For adults, there are simpler approximations, but the important point is that maintenance fluids are not resuscitation fluids.

That's the distinction I always come back to:

Resuscitation = restore perfusion and intravascular volume.

Maintenance = provide ongoing water and electrolyte requirements when the patient cannot adequately maintain them enterally.

They are fundamentally different clinical problems—and treating them as though they're the same can lead to significant complications.

So when someone says, "Let's give some fluids," my first question is:

"Are we resuscitating this patient, or are we maintaining them?"

That one distinction changes the entire conversation.

09/04/2026

ALTAVIVA: Promising Technology—or Are We Getting Ahead of the Evidence?

I’ve been looking closely at the clinical evidence behind the Medtronic Altaviva™ implantable tibial neuromodulation system for urge urinary incontinence, and I think patients deserve a little more nuance than simply hearing that “clinical trials proved it works.”

Let’s look at the actual studies.

TITAN 1 — the feasibility study

TITAN 1 ultimately implanted 20 patients. This was a small, prospective, multicenter feasibility study designed primarily to evaluate the implantation procedure and early safety/technical performance.

Twenty patients can be useful for determining whether a technology is feasible and whether there are obvious problems—but it is a very small population from which to make broad conclusions about effectiveness or long-term safety.

TITAN 2 — the pivotal study

This is where the evidence becomes more meaningful. TITAN 2 enrolled 188 patients, with 126 actually implanted. It was prospective and multicenter, but importantly, it was single-arm and nonrandomized—there was no control group against which to compare Altaviva.

At 12 months, the FDA reports a 61% clinical success rate, defined as at least a 50% reduction in daily urge urinary incontinence episodes.

That's encouraging.

But “61% responded” does not mean 61% of comparable patients in everyday practice will necessarily experience that result. Study design, patient selection, follow-up, attrition, and the absence of a randomized control group all matter.

And adverse events deserve attention as well. In the FDA-reviewed data, 20% of patients reported complications related to the device, procedure, or therapy through 12 months, with implant-site infection among the reported complications.

ENDURANCE — the long-term question

This is particularly interesting.

The FDA's post-approval ENDURANCE study is designed to evaluate long-term safety and effectiveness. The protocol anticipates enrolling approximately 256 patients to obtain at least 170 implanted subjects, accounting for anticipated attrition. It is a prospective cohort study with no comparison group and a descriptive analysis.

That tells me something important:

We are still accumulating the long-term evidence.

So is Altaviva legitimate science?

Yes.

Is it an FDA-approved technology?

Yes.

Does it have encouraging clinical data?

Yes.

But should we confuse “FDA approved” with “proven superior for most patients”?

Absolutely not.

My concern isn't that the research is fake. My concern is how confidently we extrapolate relatively limited, single-arm clinical evidence to the much larger and more heterogeneous population we see in real-world practice.

A 20-patient feasibility study is not the same evidentiary weight as a large randomized controlled trial.

A 126-patient implanted cohort without a control group cannot tell us nearly as much as a randomized comparison against established treatments.

And a post-market study still being conducted to establish longer-term durability tells us that some important questions remain open.

My honest clinical opinion?

I don't think Altaviva should be dismissed. For the appropriately selected patient with refractory urge urinary incontinence, it may be a very reasonable treatment option, particularly for someone who has failed or cannot tolerate conservative and pharmacologic therapies.

But I also wouldn't characterize it as something we can confidently recommend to most patients simply because the early studies were positive.

This is a technology I would describe as promising, legitimate, and worth watching—but still deserving of careful patient selection and continued long-term evidence.

In medicine, “new” doesn't automatically mean “better.”

And FDA approval doesn't mean we've reached the end of the evidence.

It means we have enough evidence to use the technology for its approved indication—and we should continue asking whether it truly improves outcomes compared with the alternatives.

08/31/2026

I'm Dr. Brad Medling. Five Things You Can Do to Reduce Your Risk of Kidney Stones

A little orientation before we begin: these are general recommendations that apply to most people who form calcium oxalate kidney stones. They are not a substitute for a personalized metabolic evaluation.

And there is an important distinction.

If you're 75 years old and you've just had your first kidney stone, I wouldn't obsess over it. But if you had your first stone at 16 and you've been forming another stone every 6–12 months ever since, generic advice isn't enough. You need to understand why you're forming stones.

That's where a 24-hour urine collection, such as Litholink, can be extremely helpful. It allows your clinician to identify specific abnormalities in your urine chemistry and tailor prevention to you.

With that said, here are five fundamentals:

1. Drink more water.

This is probably the single most important intervention.

The goal is to produce at least 2 liters of urine per day. For most people, that means consuming roughly 2.5 liters (about 85 ounces) of fluid daily, and potentially more if you're sweating heavily, exercising, or living in a hot environment.

The key isn't simply how much you drink—it's how much urine you produce.

2. Cut back on sodium.

A high-sodium diet increases urinary calcium excretion, a condition known as hypercalciuria, which can increase the risk of calcium-based kidney stones.

A reasonable target for most adults is 2,300 mg of sodium per day or less.

And remember: most dietary sodium doesn't come from the salt shaker. Processed foods, restaurant meals, sauces, canned foods, and packaged foods can contribute substantially.

3. Don't eliminate calcium from your diet.

This is one of the most common misconceptions.

People hear "calcium oxalate stone" and think, "I need to stop eating calcium."

Actually, dietary calcium can help bind oxalate in the gastrointestinal tract, reducing the amount of oxalate that gets absorbed and ultimately reaches the urine.

So, paradoxically, a very low-calcium diet can increase your risk of calcium oxalate stones.

The goal is generally normal dietary calcium intake, not calcium restriction.

4. Moderate your oxalate intake.

You don't necessarily need to eliminate every food containing oxalate.

Instead, look at your overall diet and identify whether you're consuming large amounts of particularly oxalate-rich foods.

And, by the way, I don't know why sweet tea has become the oxalate villain of the South. It contains oxalate, but foods such as spinach can contain dramatically higher amounts.

The point isn't necessarily "never eat this." It's moderation, particularly if you're consuming large quantities of high-oxalate foods.

5. Moderate your animal protein intake.

This one surprises people.

A diet excessively high in animal protein can alter several components of urinary chemistry—including urinary calcium, citrate, uric acid, and acid load—and can create an environment that is more favorable to stone formation.

You don't necessarily need to become vegetarian. The goal is to avoid excessive animal-protein intake and maintain a balanced diet.

The Bottom Line

These are general prevention strategies for most calcium oxalate stone formers:

💧 Hydrate adequately
🧂 Limit sodium
🥛 Maintain normal dietary calcium
🥬 Moderate high-oxalate foods
🥩 Avoid excessive animal protein

But if you're a frequent kidney-stone former, don't settle for generic advice.

If you're forming stones repeatedly—particularly at a young age—you should talk with your physician about a 24-hour urine evaluation such as Litholink. Your urine chemistry can tell you why you're forming stones and allow prevention to be tailored specifically to you.

Kidney-stone prevention isn't particularly sexy.

But it's considerably better than passing a stone.

08/29/2026

Hey Everyone! Dr. Medling here.
Hypertension is often called the “silent killer.”
Because hypertension frequently produces no obvious symptoms, people may convince themselves that nothing is wrong, that their elevated blood pressure is simply “normal for me,” or that they have plenty of time to address it later. Unfortunately, “later” often becomes years.
Persistent elevation in blood pressure creates chronic increases in systemic vascular resistance and afterload, forcing the heart to work harder with every beat. Over time, this sustained hemodynamic stress can lead to pathologic cardiac remodeling, left ventricular hypertrophy, diastolic dysfunction, and ultimately heart failure.
The kidneys are also particularly vulnerable. Chronic hypertension progressively damages the renal microvasculature and can accelerate chronic kidney disease, with some patients eventually developing severely reduced kidney function and, in advanced cases, requiring dialysis.
The important point is this: you do not have to feel sick for hypertension to be causing significant damage.
Don't wait until you develop symptoms. Don't assume that because you feel fine, your blood pressure is harmless. Work with a physician to identify the cause, assess your cardiovascular and renal risk, and get your blood pressure controlled now—not years from now.
The absence of symptoms does not mean the absence of damage.