When Medical Skepticism Becomes Conspiracy Theory

By Christopher Piercecchi, MD

SITREP is an evidence-review briefing for patients and colleagues of The Men’s Clinic for Wellness & Vitality. It is educational and does not constitute individualized medical advice.

There is a Substack titled What Else Had They Lied to Me About? that publishes under the name Lies Are Unbekoming. It describes its mission as investigating what medicine has gotten wrong, from screening and vaccines to psychiatry and chronic disease, and it has built an audience of roughly 42,000 subscribers around that premise. On its face, there is nothing objectionable about that mission. Medicine should be questioned, and its failures should be examined openly. We have prescribed treatments that later proved ineffective, screened people too aggressively, allowed financial conflicts to influence medical practice, and sometimes recommended invasive therapies more aggressively than the evidence justified. Those failures are real, and anyone defending evidence-based medicine should be willing to acknowledge them.¹

Questioning medicine is reasonable, but a recent post from this Substack titled “The 12 Diagnostic Thresholds That Were Lowered to Create Millions of New Patients” goes further and makes an accusation the evidence does not support. The writer argues that medical organizations repeatedly lowered thresholds for common conditions, simply to turn millions of previously healthy people into new patients. He then suggests a common motive: committees changed the numbers, more people became eligible for treatment, pharmaceutical markets expanded, and the decision-makers were financially connected to the companies that benefited. By the end, he tells readers that the mechanism for each change was essentially “identical in every case” and that no corresponding improvement in longevity, function, or quality of life followed.²

That is a bold claim. It argues motive, corruption, causation, and whether or not decades of preventive medicine have actually improved health, and an allegation of that size, made to tens of thousands of readers, requires evidence. The author offers no substantial evidence for his claims, and he never seriously examines why diagnostic thresholds were changed in the first place. So this SITREP will investigate whether physicians were simply redefining healthy people as sick, as the writer suggests, or whether accumulating evidence showed a legitimate need to change the thresholds for common conditions such as hypertension, obesity, diabetes, chronic kidney disease, cholesterol, osteoporosis, and prostate cancer screening.

It is true that the thresholds changed. To be diagnosed with high blood pressure you once needed a reading of 140/90, and that has been lowered to 130/80, and the same kind of change happened with obesity, diabetes, and the others. It is also true that a lot more people are now being diagnosed. But the fact that we are diagnosing more people, in and of itself, is not evidence that medicine is manufacturing disease for financial gain. The real question is whether the change is a product of science evolving, with medicine identifying disease risk earlier so we can catch disease sooner and prevent the harm it would cause later. That is where the Lies Are Unbekoming argument falls short.

He does not even entertain that possibility, and his skepticism leaves no room for it. He essentially ignores that recognizing disease earlier can prevent disease progression, complications, and premature death. Now let’s go through each of his claims and take a look at them individually.

Hypertension

The first major example in the Lies Are Unbekoming post is hypertension. The writer points out that the 2017 ACC/AHA guideline changed the definition of hypertension from 140/90 to 130/80 mmHg³ and emphasizes that millions of Americans who had not previously been classified as hypertensive suddenly met the new definition. He describes approximately 31 million people as essentially becoming sick overnight because a committee moved a number.² No one disputes that the definition changed or that the change increased the number of people classified as hypertensive. The conclusion he draws from that fact is wrong. He treats the previous cutoff of 140/90 as though it represented some established biological boundary that medicine later abandoned for suspicious reasons, when the more important question is whether the older threshold was actually doing a good enough job of identifying cardiovascular risk.

This is also a good place to remember how science is supposed to work. We continually study outcomes, test earlier assumptions, collect better data, and revise our understanding when the evidence tells us that the old model was incomplete. Blood pressure is a perfect example. As larger datasets and better clinical trials accumulated, we learned more about the cardiovascular consequences of spending years with pressures that had previously been considered acceptable. That new information allowed us to identify risk earlier and refine when intervention might be worthwhile. Treating every revision of a medical threshold as evidence of something nefarious turns the scientific process on its head. If medicine never changed its definitions, recommendations, or treatments when better evidence became available, that would not be a sign of integrity. It would be a sign that we had stopped learning. Humanity has advanced because we revise what we think we know when the evidence improves; otherwise, we would still be banging rocks together to light a fire.

And that is exactly what the blood-pressure data were showing. Cardiovascular risk does not suddenly appear when systolic pressure reaches 140 mmHg; it rises progressively across the blood-pressure range. By the time the guideline changed, substantial evidence showed that people with pressures below the old hypertension threshold still experienced higher rates of stroke, myocardial infarction, heart failure, and other cardiovascular disease. The SPRINT Trial then added randomized evidence that treating blood pressure more intensively in appropriately selected higher-risk adults could improve clinical outcomes. The trial found roughly a 25% reduction in its major cardiovascular composite with more intensive treatment, although adverse effects such as hypotension, electrolyte disturbances, and acute kidney injury were also more common.⁴

What did we gain by recognizing hypertension earlier? We gained years in which patients could lower their blood pressure through weight loss, regular exercise, improved sleep, reduced alcohol intake, and, when their cardiovascular risk justified it, medication. None of this meant that everyone with a blood pressure of 130/80 suddenly needed a prescription. The guideline still considered the patient’s overall cardiovascular risk, and lifestyle intervention remained the initial approach for many lower-risk people. The lower threshold was therefore not simply a way of expanding the treated population; it allowed physicians to recognize cardiovascular risk earlier, while there was still time to do something about it.

That is the part of the story the Lies Are Unbekoming writer largely skips. Whether that omission reflects selective framing or simply a poor understanding of how scientific evidence and guideline development actually work, the result is the same: he focuses on the increase in the number of people carrying the diagnosis while giving far less attention to the cardiovascular risk the older definition was failing to capture. His broader claim about financial influence also runs into trouble here. The 2017 ACC/AHA hypertension guideline reported that no member of the writing committee had a relevant relationship with industry.³ Conflicts of interest have certainly affected medicine and deserve scrutiny when they occur, but this particular example does not fit the uniform pharmaceutical mechanism he claims is operating throughout the article.

Obesity

The writer makes the same argument about BMI, presenting a change in a category boundary as evidence that healthy people were turned into patients. In 1998, the U.S. adopted a BMI of 25 as the beginning of the overweight category, replacing higher sex-specific thresholds that had previously been used.⁵ Millions of Americans consequently moved into the overweight category. He then jumps forward more than two decades and points to the enormous modern GLP-1 market as the eventual “commercial payoff” from that decision.

The way he tells this story leaves the impression that the definition of obesity was lowered, and that is wrong. The threshold for obesity did not change. A BMI of 25 became the lower boundary of the overweight category, while obesity still began at BMI 30.⁵ His post never explains that distinction clearly, so a reader who does not already know the difference between overweight and obese would reasonably come away believing medicine moved the line for obesity itself, when what actually changed was where the overweight category begins. The accusation depends on that confusion, which makes the omission far more than a minor oversight.

Before accepting the rest of his interpretation, it also helps to be clear about what the 1998 guideline recommended. It did not call for medication for everyone whose BMI crossed 25. For people in the overweight range, the emphasis was largely on identifying additional cardiometabolic risk and addressing weight through nutrition, physical activity, and other lifestyle measures, particularly when increased waist circumference or other risk factors were present.⁵

Why move the threshold at all? Because the old categories were doing a poor job of reflecting what population data were showing about health risk. Cardiometabolic risk does not suddenly begin when BMI reaches 30. Rates of type 2 diabetes, hypertension, dyslipidemia, and cardiovascular disease were already increasing through the overweight range, particularly when excess abdominal fat was present.⁵ Recognizing that someone had entered a higher-risk range gave physicians and patients an opportunity to address weight, fitness, blood pressure, glucose, and other metabolic factors before obesity and its complications became more established. That is not creating disease. It is recognizing risk earlier, while there is still more opportunity to change its trajectory.

The attempt to connect the 1998 change to today’s GLP-1 market is weaker still. A BMI of 25 by itself does not qualify someone for contemporary anti-obesity medication; those indications generally begin with obesity or with overweight accompanied by an obesity-related medical condition.⁶ More importantly, the classification change occurred more than twenty years before the modern GLP-1 obesity market emerged. The fact that profitable medications later incorporated BMI into their eligibility criteria does not tell us why the 1998 committee changed the classification. To make that argument, the writer would need evidence that the earlier threshold was established for the purpose of creating a future treatment market. He does not provide it.

Diabetes

Diabetes is the next example, and the post criticizes the 1997 decision to lower the fasting glucose threshold from 140 to 126 mg/dL.⁷ The post’s framing is that people with fasting glucose values between 126 and 139 had been considered normal, a committee changed the number, and suddenly millions of people had diabetes. Presented that way, the change sounds arbitrary. But the important question is why the old threshold was changed, and this is where his argument again becomes much less persuasive.

The previous cutoff of 140 mg/dL was not doing a particularly good job of identifying the point at which diabetic complications were already beginning to appear. When investigators examined the relationship between fasting glucose and diabetic retinopathy, they found that retinopathy prevalence began to rise at glucose levels closer to 126 mg/dL.⁷ The expert committee also wanted the fasting-glucose criterion to correspond more closely with the established two-hour oral glucose-tolerance criterion.⁷ In other words, the threshold did not move because someone simply decided that 126 looked better than 140. It moved because the accumulating data suggested that clinically important diabetic injury was already appearing below the old cutoff.

That is the health consequence the original post largely ignores. If retinal microvascular damage is already becoming more common before fasting glucose reaches 140, continuing to call everyone below 140 “normal” does not make those people healthier. It simply delays recognition of a metabolic disorder that is already beginning to cause harm. Identifying diabetes earlier gives patients and physicians more time to address weight, nutrition, physical activity, blood pressure, lipids, and glycemic control before years of additional hyperglycemia accumulate and before complications become more established.

The same reasoning applies, with more caution, to prediabetes. Prediabetes is not diabetes, and it should not be presented to patients as though progression is inevitable. Many people with mildly abnormal glucose values will never develop diabetes, and the label can certainly be overused. But the category identifies a population whose likelihood of progressing is meaningfully higher and, importantly, whose trajectory can often be changed.

The Diabetes Prevention Program demonstrated why that information can be useful. Among 3,234 adults at high risk for diabetes, intensive lifestyle intervention reduced the incidence of diabetes by 58% compared with placebo and was substantially more effective than metformin.⁸ Roughly seven people needed to participate in the lifestyle program for three years to prevent one case of diabetes.⁸ That result is particularly inconvenient for the argument that expanding these categories was principally about expanding pharmaceutical markets. The most effective intervention in the landmark prevention trial was not a new drug. It was weight loss, nutrition, and physical activity.

Chronic Kidney Disease

Chronic kidney disease is where the post makes its most defensible point. Kidney filtration declines with age, and using a fixed eGFR threshold below 60 can overstate the significance of modest reductions in kidney function in some older adults.⁹ An otherwise healthy 80-year-old with a stable eGFR of 55 and no albuminuria is not in the same clinical situation as a younger patient with the same eGFR, heavy albuminuria, and progressive decline. That criticism is fair, but he stretches it into a claim that CKD staging mainly created a new population of patients who could then be monitored and treated with drugs.

That conclusion misses why earlier recognition of kidney disease matters in the first place. Chronic kidney disease can remain clinically silent while renal function is gradually being lost, which means waiting for symptoms is a poor strategy. Modern CKD assessment also does not treat every person with an eGFR below 60 as though the prognosis were the same. Albuminuria, the underlying cause, the duration of the abnormality, the trajectory of kidney function, and the rest of the clinical picture all help determine who is actually at substantial risk of progression.¹⁰

Recognizing higher-risk CKD earlier gives us time to act before more renal function is lost. We can improve blood-pressure control, identify and treat albuminuria, manage diabetes more aggressively, avoid nephrotoxic exposures, adjust medications, address the underlying renal disease when possible, and use kidney-protective therapies in patients who are likely to benefit. The point is not simply to attach a diagnosis to a laboratory value. It is to preserve kidney function while there is still kidney function left to preserve.

The outcome data support that approach. In DAPA-CKD, dapagliflozin reduced the composite of major kidney-function decline, end-stage kidney disease, or renal or cardiovascular death from 14.5% to 9.2% over approximately 2.4 years, an absolute reduction of 5.3 percentage points, with benefit in patients both with and without diabetes.¹¹ Those are clinically meaningful outcomes, not merely changes in creatinine or eGFR.

So the writer is right that we should be careful about overinterpreting a mildly reduced eGFR in an older adult and about applying the same label too rigidly across very different patients. But that is not evidence that CKD staging was created to manufacture pharmaceutical customers. Earlier recognition helps us identify the patients who are actually at risk and intervene before they arrive with advanced renal disease.

Cholesterol Targets

The most direct accusation of profit motive is aimed at cholesterol treatment. The post portrays progressively lower LDL thresholds as a way of growing the market for statins, ezetimibe, PCSK9 inhibitors, and other lipid-lowering therapies while delivering little meaningful health benefit. He points to the expanding treatment population as though that expansion itself demonstrates what motivated the guideline changes. What he largely leaves out is why lipidology has become more aggressive in the first place: we have learned considerably more about how atherosclerosis develops and how much cumulative exposure to apoB-containing lipoproteins matters over a lifetime.

Atherosclerosis does not suddenly appear shortly before someone has a heart attack. It develops quietly over decades as apoB-containing particles, including LDL particles, enter and become retained within the arterial wall. That means the cholesterol exposure someone accumulates in his twenties, thirties, and forties matters to the plaque burden he carries later in life.¹²,¹³ This is why modern prevention is increasingly concerned not only with a person’s 10-year cardiovascular risk, but with lifetime exposure to LDL and apoB. A younger person with an LDL of 120 mg/dL may have a very low short-term risk simply because he is young, but decades of elevated atherogenic exposure are not biologically irrelevant, particularly when family history, Lp(a), apoB, smoking, diabetes, hypertension, or other risk factors are present.

The clinical trial evidence also directly contradicts the suggestion that pushing LDL lower merely sells more medication without improving outcomes. Large statin trials consistently showed fewer major vascular events as LDL was reduced.¹⁴ IMPROVE-IT then demonstrated that lowering LDL further with ezetimibe after acute coronary syndrome reduced cardiovascular events beyond statin therapy alone.¹⁵ FOURIER pushed achieved LDL much lower, to a median of approximately 30 mg/dL, and again produced fewer major cardiovascular events.¹⁶ These were not simply improvements in a laboratory number. They were fewer heart attacks, strokes, and related cardiovascular events.

That is why treatment goals have become more aggressive, particularly in people at higher risk. We learned that patients continued to experience preventable events at LDL levels that had once been considered adequately treated, while newer evidence increasingly supported the importance of reducing cumulative apoB exposure earlier in life. The Lies Are Unbekoming post also gets part of the chronology wrong when it claims that the 2018 ACC/AHA guideline established an LDL target below 55 mg/dL for very-high-risk patients. It did not. The 2018 guideline used 70 mg/dL as the threshold for considering additional nonstatin therapy in very-high-risk ASCVD; the more aggressive U.S. target came later as additional evidence accumulated.¹⁷,¹⁸

The stakes are higher here because lipid-lowering therapy rests on some of the strongest outcome evidence in preventive medicine, and the post gives that evidence little weight. It sees lower targets, more treatment, and newer medications and concludes that the purpose must be to create customers, while giving little attention to the disease process those treatments interrupt or to the randomized trials showing fewer cardiovascular events when they do. Readers who come away believing that lowering cholesterol is unnecessary, harmful, or merely another pharmaceutical scheme may decline or stop treatments that have been shown to prevent heart attacks and strokes, and some of those decisions will have real consequences.

Bone Density

Osteopenia is another place where the post raises a legitimate concern. A T-score between -1.0 and -2.5 describes bone density relative to a young-adult reference population, and that number alone should not turn someone into a patient who automatically needs medication. If his argument stopped there, there would be plenty to agree with. He overreaches by taking a reasonable criticism about overdiagnosis and using it to suggest that the broader effort to identify low bone density was essentially another exercise in creating disease and expanding treatment.

What that framing leaves out is why bone-density testing became useful in the first place. Osteoporosis is often clinically silent until the first fragility fracture occurs, and by then an important opportunity for prevention has already been lost. A hip or vertebral fracture in an older adult can lead to chronic pain, loss of mobility, loss of independence, and substantial morbidity.¹⁹ The purpose of identifying skeletal fragility earlier is to recognize the people at greatest fracture risk before the fracture becomes the event that finally reveals the problem.

In practice, nobody should be making a treatment decision from the T-score alone. A woman with mild osteopenia, no prior fractures, and otherwise low fracture risk is very different from an older woman with the same T-score who has already sustained a fragility fracture, falls frequently, or has other factors that substantially increase her risk. That is why clinicians look at the whole picture before deciding whether treatment is warranted.²⁰ The Lies Are Unbekoming post largely skips over that clinical judgment and instead makes it sound as though once the DEXA scan produces the word “osteopenia,” a prescription inevitably follows. That is simply not how appropriate osteoporosis management works.

The writer goes further by arguing that bisphosphonates essentially create the problem they are supposed to prevent because prolonged suppression of bone turnover can contribute to atypical femoral fractures and osteonecrosis of the jaw. Those adverse effects deserve attention, and they are exactly why patient selection and treatment duration matter.²⁰,²¹ What he gives far less attention to is the other half of the evidence: randomized trials show that bisphosphonates substantially reduce ordinary osteoporotic fractures in appropriately selected high-risk patients.²² Focusing on uncommon treatment complications while largely ignoring the fractures prevented by treatment produces a badly distorted picture of the risk-benefit calculation.

The number of people who receive an osteopenia label is not, by itself, the outcome that matters. The relevant question is whether we are distinguishing low-risk patients who do not need medication from people whose fracture risk is high enough that intervention is likely to help. The objective is not to manufacture an osteoporosis patient from a DEXA scan; it is to identify skeletal fragility early enough that the first sign of the disease does not have to be a hip fracture.

PSA Screening

PSA screening is offered as one more example of medicine expanding a disease category and pulling healthy men into testing, biopsy, and treatment. The post focuses on the historical PSA cutoff of 4.0 ng/mL and on subsequent efforts to lower the threshold toward 2.5, arguing that doing so would inevitably send millions of additional men into the biopsy cascade. There is a legitimate criticism here. The old approach to PSA screening was crude, and treating a single cutoff as a near-automatic trigger for biopsy produced false positives, unnecessary procedures, overdiagnosis of indolent cancers, and treatment of some tumors that never would have harmed the patient.

But the failures of the old screening model do not make earlier detection of prostate cancer a bad idea. A PSA of 4.0 is not some biological boundary below which significant prostate cancer does not exist, and waiting for a man’s PSA to cross an arbitrary number can mean missing aggressive disease while it is still localized and potentially curable. Modern evaluation is much better at dealing with that problem. An elevated PSA can be repeated, and age, family history, PSA density, biomarkers, risk calculators, MRI findings, and other clinical information can help determine which men are actually likely to harbor clinically significant cancer before anyone proceeds to biopsy.²³

The objective today is not simply to find as much prostate cancer as possible. It is to become better at finding the cancers that matter while avoiding unnecessary intervention for the ones that do not. Randomized screening data support that effort. In the European Randomized Study of Screening for Prostate Cancer, PSA-based screening reduced the incidence of metastatic prostate cancer, and longer follow-up showed a reduction in prostate-cancer mortality.²⁴,²⁵ Screening therefore did more than create additional diagnoses. It shifted some cancers toward an earlier stage, when treatment has a much better chance of being curative.

The U.S. experience after PSA screening declined is also worth considering. Following recommendations that discouraged routine screening, PSA testing fell substantially, and subsequent registry data showed rising rates of metastatic prostate cancer at diagnosis.²⁶ That observation by itself cannot prove that reduced screening caused the increase, and it should not be presented that way. But it is difficult to dismiss when randomized trials independently show that screening can reduce metastatic disease. Taken together, the evidence argues for better and more selective screening, not for abandoning the effort to find dangerous cancers early.

The phrase “creating sick people” is especially misleading in the PSA discussion. Screening will identify more prostate cancers because that is what screening is designed to do. Some of those cancers will be indolent, which is why active surveillance and better risk stratification are so important. Others are aggressive cancers that may still be confined to the prostate when they are discovered but could eventually present with nodal, bone, or visceral metastases if nobody looks for them. Those men were not made sick by the PSA test. They were made sick by the cancer. The purpose of modern screening is to find clinically significant disease while we still have the opportunity to cure it and, at the same time, become better at leaving low-risk disease alone.

Where the Argument Breaks Down

The central problem with the Lies Are Unbekoming post is not that every historical fact in it is false. Many of them are true. Diagnostic thresholds changed. More people met disease or risk definitions afterward. Medication use increased. Some guideline committees have had troubling financial relationships, and medicine has unquestionably produced examples of overdiagnosis and overtreatment.¹ There are cases where medicine went too far, and those failures deserve scrutiny.

What does not follow is the conclusion the writer repeatedly draws from those facts. A threshold changes, more people are identified, and treatment subsequently increases. He then treats that sequence as evidence that the threshold was changed in order to create customers for the treatment. Showing that pharmaceutical markets expanded after a guideline change does not establish that expanding those markets was the reason the guideline changed. If you are going to make a claim about motive and corruption, you need evidence of motive and corruption. Chronology alone does not provide it.

The examples we have examined throughout this piece offer far better explanations for why many of these recommendations changed. Blood-pressure criteria moved because cardiovascular risk exists below 140/90. Diabetes criteria changed because microvascular injury was appearing below the old fasting-glucose threshold. CKD staging allows progressive renal disease to be recognized before substantial kidney function has been lost. Lipid recommendations have become more aggressive because atherosclerosis reflects cumulative exposure to apoB-containing particles and cardiovascular events decline when that exposure is reduced. Bone-density screening attempts to identify substantial fracture risk before the fracture occurs, and modern PSA screening tries to find clinically significant prostate cancer before it becomes metastatic.

That tension is built into preventive medicine. Looking earlier will inevitably identify some people who would never have progressed to a meaningful clinical problem, which is why overdiagnosis deserves serious attention and why screening strategies and treatment thresholds should continue to evolve. But acknowledging that limitation does not mean the better alternative is to wait until disease becomes obvious.

We could create fewer hypertension patients by waiting until people had strokes. We could create fewer diabetes patients by waiting for retinopathy or nephropathy, fewer CKD patients by waiting for advanced renal failure, fewer osteoporosis patients by waiting for hip fractures, and fewer localized prostate cancer patients by waiting until the disease had spread. The charts would contain fewer diagnoses, but the people represented by those charts would not be healthier. Preventive medicine exists precisely because waiting until disease announces itself through irreversible injury is often too late.

When Skepticism Becomes a Worldview

The post’s individual errors reflect a broader flaw in how the Substack approaches these questions. Skepticism is essential to science, but scientific skepticism means testing a claim, examining competing explanations, and being willing to change your mind when the evidence points somewhere you did not expect. It does not mean beginning with the assumption that institutions are deceiving you and then interpreting each new fact through that assumption.

The framing of The Lies Are Unbekoming Substack itself makes that orientation fairly explicit. It is called What Else Had They Lied to Me About? The reader is being invited to approach medicine and other institutions with the presumption that something has been hidden from him and that the writer is now uncovering what really happened. That is a powerful rhetorical position because it asks the reader to distrust the people and institutions generating the medical evidence while simultaneously trusting the person accusing them of deception. A writer who asks readers to trust him over those institutions should be held to a higher standard of evidence, not a lower one.

The danger is that once this framework is adopted, almost any new information can be made to confirm it. Evidence supporting the writer’s suspicion becomes proof that the system is compromised. Evidence that does not fit can be dismissed as coming from the same compromised system. That creates a closed loop in which the original assumption becomes increasingly difficult to challenge, not because it has survived rigorous testing, but because contradictory evidence has been disqualified in advance.

That is not how scientific skepticism is supposed to function. The same standard of evidence should apply whether a claim comes from a pharmaceutical company, a professional society, an academic researcher, or a Substack writer telling tens of thousands of people that those institutions cannot be trusted. Criticism of medicine does not become more credible simply because it is anti-establishment, and suspicion is not evidence.

This matters because these arguments do not remain confined to abstract debates about guidelines. Readers may change what they do with their health based on what they are told. If someone is persuaded that preventive treatment is mostly a scheme, he may decline therapy, abandon screening, or stop a medication that was reducing a meaningful risk. People are free to make those decisions, but they should make them from an accurate understanding of the evidence rather than from a narrative in which every recommendation is presumed guilty before it is examined.

Medicine deserves criticism when it gets things wrong. It also deserves a fair reading of the evidence when it gets something right. Skepticism should protect us from weak claims, not become a reason to reject strong evidence simply because accepting it would spoil the story.

References

1. Neuman J, Korenstein D, Ross JS, Keyhani S. Prevalence of financial conflicts of interest among panel members producing clinical practice guidelines in Canada and United States: cross sectional study. BMJ. 2011;343:d5621. doi:10.1136/bmj.d5621.

2. Unbekoming. “The 12 Diagnostic Thresholds That Were Lowered to Create Millions of New Patients.” Lies Are Unbekoming. September 6, 2026.

3. Whelton PK, Carey RM, Aronow WS, et al. 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults. Circulation. 2018;138(17):e484-e594. doi:10.1161/CIR.0000000000000596.

4. SPRINT Research Group. A Randomized Trial of Intensive versus Standard Blood-Pressure Control. N Engl J Med. 2015;373:2103-2116. doi:10.1056/NEJMoa1511939.

5. National Heart, Lung, and Blood Institute Obesity Education Initiative Expert Panel. Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report. Bethesda, MD: National Heart, Lung, and Blood Institute; 1998.

6. U.S. Food and Drug Administration. FDA Approves New Medication for Chronic Weight Management. November 8, 2023.

7. Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care. 1997;20(7):1183-1197. doi:10.2337/diacare.20.7.1183.

8. Diabetes Prevention Program Research Group. Reduction in the Incidence of Type 2 Diabetes with Lifestyle Intervention or Metformin. N Engl J Med. 2002;346:393-403. doi:10.1056/NEJMoa012512.

9. Delanaye P, Glassock RJ, Pottel H, Rule AD. An Age-Calibrated Definition of Chronic Kidney Disease: Rationale and Benefits. Clin Biochem Rev. 2016;37(1):17-26.

10. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S):S117-S314. doi:10.1016/j.kint.2023.10.018.

11. Heerspink HJL, Stefánsson BV, Correa-Rotter R, et al. Dapagliflozin in Patients with Chronic Kidney Disease. N Engl J Med. 2020;383:1436-1446. doi:10.1056/NEJMoa2024816.

12. Zhang Y, Pletcher MJ, Vittinghoff E, et al. Association Between Cumulative Low-Density Lipoprotein Cholesterol Exposure During Young Adulthood and Middle Age and Risk of Cardiovascular Events. JAMA Cardiol. 2021;6(12):1406-1413. doi:10.1001/jamacardio.2021.3508.

13. Zheutlin AR, Handoo F, Luebbe S, et al. Cumulative exposure to atherogenic lipoprotein particles in young adults and subsequent incident atherosclerotic cardiovascular disease. Eur Heart J. 2025;46(41):4302-4312. doi:10.1093/eurheartj/ehaf472.

14. Cholesterol Treatment Trialists’ (CTT) Collaboration. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670-1681. doi:10.1016/S0140-6736(10)61350-5.

15. Cannon CP, Blazing MA, Giugliano RP, et al. Ezetimibe Added to Statin Therapy after Acute Coronary Syndromes. N Engl J Med. 2015;372:2387-2397. doi:10.1056/NEJMoa1410489.

16. Sabatine MS, Giugliano RP, Keech AC, et al. Evolocumab and Clinical Outcomes in Patients with Cardiovascular Disease. N Engl J Med. 2017;376:1713-1722. doi:10.1056/NEJMoa1615664.

17. Grundy SM, Stone NJ, Bailey AL, et al. 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol. Circulation. 2019;139:e1082-e1143. doi:10.1161/CIR.0000000000000625.

18. American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia. Circulation. 2026;153:e1154-e1276. doi:10.1161/CIR.0000000000001423.

19. U.S. Preventive Services Task Force. Osteoporosis to Prevent Fractures: Screening. Final Recommendation Statement. January 14, 2025.

20. Eastell R, Rosen CJ, Black DM, Cheung AM, Murad MH, Shoback D. Pharmacological Management of Osteoporosis in Postmenopausal Women: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2019;104(5):1595-1622. doi:10.1210/jc.2019-00221.

21. Black DM, Geiger EJ, Eastell R, et al. Atypical Femur Fracture Risk versus Fragility Fracture Prevention with Bisphosphonates. N Engl J Med. 2020;383:743-753. doi:10.1056/NEJMoa1916525.

22. Liberman UA, Weiss SR, Bröll J, et al. Effect of Oral Alendronate on Bone Mineral Density and the Incidence of Fractures in Postmenopausal Osteoporosis. N Engl J Med. 1995;333:1437-1443. doi:10.1056/NEJM199511303332201.

23. Wei JT, Barocas D, Carlsson S, et al. Early Detection of Prostate Cancer: AUA/SUO Guideline. J Urol. 2023;210(1):46-53. doi:10.1097/JU.0000000000003491.

24. Schröder FH, Hugosson J, Carlsson S, et al. Screening for Prostate Cancer Decreases the Risk of Developing Metastatic Disease: Findings from the European Randomized Study of Screening for Prostate Cancer (ERSPC). Eur Urol. 2012;62(5):745-752. doi:10.1016/j.eururo.2012.05.068.

25. Hugosson J, Roobol MJ, Månsson M, et al. A 16-yr Follow-up of the European Randomized Study of Screening for Prostate Cancer. Eur Urol. 2019;76(1):43-51. doi:10.1016/j.eururo.2019.02.009.

26. Desai MM, Cacciamani GE, Gill K, et al. Trends in Incidence of Metastatic Prostate Cancer in the US. JAMA Netw Open. 2022;5(3):e222246. doi:10.1001/jamanetworkopen.2022.2246.

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