2.1 OCD List

Rethinking “Pre-Diabetes”

Pre-diabetes is not a warning sign before disease. It is an early form of diabetes.

The term pre-diabetes suggests a harmless waiting room — a stage before “real” damage begins. That framing is misleading.

By the time someone meets criteria for pre-diabetes, organ and vascular injury are already underway.

What the science shows:

• Blood vessels:
  People with pre-diabetes already show endothelial dysfunction, increased arterial stiffness, and early atherosclerotic changes. These abnormalities predict future cardiovascular disease, even if diabetes never develops.
• Heart:
  Subclinical changes in cardiac structure and function (including impaired diastolic relaxation) are detectable in pre-diabetes, increasing long-term heart-failure risk.
• Kidneys:
  Microalbuminuria and early declines in renal function occur more frequently in people with pre-diabetes than in metabolically healthy controls.
• Nerves:
  Small-fiber neuropathy and autonomic nerve dysfunction have been documented in pre-diabetes, often before overt diabetes is diagnosed.
• Brain:
  Insulin resistance and glucose dysregulation at the pre-diabetic stage are associated with cognitive decline, white-matter changes, and increased risk of dementia later in life.
• Risk trajectory:
  Cardiovascular risk rises continuously with glucose and insulin levels — there is no safe threshold where damage suddenly begins at the diabetes cutoff.

In other words, pre-diabetes reflects a system already under metabolic stress with measurable consequences. It is NOT a benign precursor state.

(In clinical practice, when I ask someone if they have diabetes, I often hear No, just pre-diabetes. That just misses the fact that chronic inflammation and organ damage are already underway.)

Why the language matters:
Calling this stage “pre-diabetes” delays urgency, reassurance replaces action, and opportunities for true prevention are missed.

A more accurate framing is: Early diabetes with preserved glucose compensation.

Triglycerides — Fasting vs. Non-Fasting (What Each One Really Tells You)

Triglycerides are dynamic.
They rise and fall based on what you ate, when you ate, and how well your metabolism handles fat.

Understanding when they’re measured changes what they mean.

What Triglycerides Actually Represent

Blood triglycerides reflect fat in transit, not fat stored in adipose tissue.

After a meal:

• Dietary fat is packaged into chylomicrons
• These circulate, deliver fat to tissues, and are gradually cleared

But this process isn’t rapid or tidy.

A Key Update to the Old Teaching

It was once assumed that chylomicrons appear after a meal–>circulate briefly–>disappear within a few hours.

We now know:

• Chylomicrons and especially chylomicron remnants can persist for many hours
• Some lipid particles remain in intestinal lymphatics and enter circulation later
• With frequent meals, many people spend much of the day in a post-prandial lipid state

In insulin resistance, clearance is slower — so triglyceride-rich particles accumulate across meals.

Why Non-Fasting Triglycerides Gained Acceptance

Large population studies showed that non-fasting triglycerides:

• predict cardiovascular events and stroke
• reflect real-world exposure of blood vessels to triglyceride-rich lipoproteins
• capture remnant particle burden better than a single fasting snapshot

From a population cardiovascular-risk perspective, this was the rationale.

Non-fasting triglycerides answer the question, how much triglyceride traffic do your blood vessels see across the day?

What Fasting Triglycerides Show (That Non-Fasting Can’t)

After a 10–12 hour fast:

• Chylomicrons are largely cleared
• Triglycerides mainly reflect hepatic VLDL production

Elevated fasting triglycerides suggest:

• hepatic insulin resistance
• increased liver fat
• excess de novo lipogenesis
• impaired suppression of lipid release by insulin

This is why fasting triglycerides track closely with:

• TAG:HDL ratio
• fasting insulin
• HOMA-IR
• fatty liver risk

Fasting triglycerides answer the question how stressed is the liver at baseline?

Why Both Can Be True

These two measurements are not competitors.

• Non-fasting TGs → cumulative daily lipid exposure & vascular risk
• Fasting TGs → hepatic fat handling & metabolic compensation

Which one matters more depends on what you are trying to understand.

Why Fasting Matters for Metabolic Insight

When triglycerides are used to:

• assess insulin resistance
• calculate TAG:HDL ratio
• interpret liver fat dynamics

Fasting conditions provide a cleaner signal.

Non-fasting values may still be informative — but they require context. That’s why I have my patients fast for this test.

Takeaway

• If your goal is cardiovascular screening, non-fasting lipids are often sufficient.
• If your goal is metabolic understanding, request a 12-hour fasting lipid panel.
• Interpret triglycerides alongside HDL, insulin, and glucose patterns — never alone.

How CGMs Work (and How to Use Them Wisely)

CGMs do not measure blood glucose.
They measure glucose in the interstitial fluid — the fluid that surrounds your cells.

That distinction matters.

Blood vs. Interstitial Glucose (Why the Curves Lag)

• Blood glucose rises first after a meal.
• Interstitial glucose reflects what has moved out of the bloodstream and into tissues.

As a result:

• CGM readings typically lag blood glucose by ~5–15 minutes.
• Rapid spikes or drops may appear delayed or slightly blunted on a CGM.

This is normal physiology — not device error.

For pattern recognition, this delay is acceptable — even helpful.
For acute medical decisions, it is not.

What CGMs Are Good For

CGMs excel at:

• revealing patterns, not point values
• showing relative responses to foods, stress, sleep, and movement
• identifying volatility (spikes, crashes, prolonged elevations)

They are best used as learning tools, not diagnostic instruments.

What CGMs Are Not For

Especially with over-the-counter CGMs (e.g., wellness-focused devices):

• They should not be used for:
  • diagnosing diabetes
  • adjusting medications
  • making urgent medical decisions

About Soreness or Discomfort After Removal

Some people report localized soreness after CGM removal.

What’s likely happening:

• The sensor filament sits in subcutaneous tissue, near small nerves and muscle fascia.
• Muscle contraction during self-removal (e.g., reaching behind the arm and activating the triceps) may tug on tissue during withdrawal.
• Removing the sensor with the arm relaxed and supported may reduce post-removal soreness.

This is a plausible mechanical explanation — not a sign of tissue injury.

Persistent pain, redness, or swelling is not expected and should be evaluated.

Setting Expectations

CGMs are powerful mirrors — not judges.

A spike is not a failure. A flat line is not virtue.

The goal is understanding how your body responds — not chasing “perfect” numbers.

In short, CGMs measure interstitial glucose, not blood, making them excellent for pattern recognition, but inappropriate for medical decision-making without supervision.

When “Normal” Keeps Moving

If you’ve been around medicine long enough, you may remember a time when:

• Post-meal glucose >120 mg/dL raised concern
• Later, 140 mg/dL became the accepted upper bound
• Today, you’ll often hear that up to 180 mg/dL after meals is “acceptable” in modern clinical practice

This shift deserves scrutiny.

1. The thresholds didn’t rise because human physiology changed

Our cells did not suddenly become more tolerant of glucose.

What did change:

• average calorie intake
• meal size and frequency
• carbohydrate density
• baseline insulin resistance across the population

As metabolic disease became more common, the definition of “normal” drifted to match the population, not ideal physiology.

2. Rising thresholds parallel rising disease burden

The timeline is striking:

• As post-meal glucose cutoffs rose, so did:
  • obesity prevalence
  • type 2 diabetes
  • fatty liver disease
  • cardiovascular disease

This doesn’t prove causation — but it does suggest that “normal” has become a statistical average, not a marker of metabolic health. Another way to think about this is that if you’re “normal”, you’re as unhealthy as most people.

3. These cutoffs are pragmatic, not sacred

The 180 mg/dL post-prandial threshold is not a biological cliff.
It’s a clinical compromise.

Why it exists:

• to manage population-level care
• to avoid labeling a majority of adults as metabolically abnormal (even if it’s true)
• to focus limited resources on those at highest immediate risk

This makes sense for public health triage.
It is far less satisfying for personal physiology.

4. CGMs expose what population medicine smooths over

Continuous glucose monitoring reveals something clinic snapshots miss:

• large post-meal excursions
• repeated daily spikes
• prolonged time above baseline

Even when fasting glucose and A1c are “normal.”

From a CGM perspective, the question is not did you cross a diagnostic threshold ? but how often, how high, and how long does your glucose remain elevated?

That’s a different — and more nuanced — question.

5. The uncomfortable implication

If we held post-meal glucose targets at 120 mg/dL, many modern eating patterns would immediately appear excessive.

That’s not a moral judgment. It’s a metabolic reality.

Raising thresholds has, in part, allowed us to:

• normalize overconsumption
• delay intervention
• frame disease as inevitable rather than cumulative

Again: this is not about blame — it’s about honesty. It’s easier to get an A in your metabolic health because we lowered the bar, not because you got any healthier. If you’re wondering why we’re getting sicker and sicker it’s because our standards reflect what we get in life (and health).

Takeaway

• Higher post-meal glucose targets reflect population management, not optimal biology.
• A CGM is not meant to enforce perfection, but to reveal patterns.
• Occasional excursions happen. Chronic, repeated spikes matter more than any single number.