“Your LDL is high. You’ll get a heart attack”.
That’s the fear most people live with.But science says something very different.
Here’s the most important thread you’ll read on LDL cholesterol:
Myths, truths, risks, and what REALLY matters. 🧵👇
1. LDL is not “bad cholesterol.”
LDL (Low-Density Lipoprotein) is not cholesterol.
It’s a carrier vehicle that transports cholesterol from the liver to cells.
Every cell needs cholesterol to:
•Build membranes
•Make sex hormones
•Produce bile & vitamin D
⚠️ LDL is a delivery system, not a toxin.
2. What makes LDL dangerous? Not quantity.But quality.
LDL becomes risky when it’s:
⚠️ Oxidized (damaged)
⚠️ Small & dense (easily trapped in arteries)
⚠️ High in number (ApoB)
⚠️ In an environment of inflammation + insulin resistance
LDL is like a delivery truck. Problem isn’t the truck, it’s damaged trucks in a traffic jam on a broken road.
3. What LDL levels are considered “safe” around the world?
🔻 < 100 mg/dL → general public
🔻 < 70 mg/dL → diabetics or those with heart disease
🔻 < 55 mg/dL → recent heart attack/stroke survivors
But here’s the twist ⤵️
4. Ultra-low LDL isn’t always better.
🧠 Studies show LDL < 70 may be linked to:
Increased hemorrhagic stroke
Higher mortality in elderly
Cognitive decline in some cases
📚 Especially in malnourished, insulin-deficient, or underweight populations.
🔁 So lower is not universally better. Context matters.
5. ApoB is the real silent killer And not LDL-C.
🧪 ApoB = # of atherogenic particles (LDL, VLDL, IDL, Lp(a))
Each particle = 1 ApoB
So it tells you how many particles are roaming your blood
📌 Many people with “normal” LDL still have high ApoB → hidden danger.
6. Size matters: Small dense LDL = dangerous.
🔴 Small, dense LDL → enters artery walls → oxidized → triggers plaque
🟢 Large, fluffy LDL → less likely to cause problems
What causes small LDL particles?
❌ High sugar intake
❌ Refined carbs
❌ Low HDL
✅ Fixed by: low-carb diet, exercise, and fixing insulin resistance
7. The #1 enemy of your heart is not LDL . It’s insulin resistance.
High insulin causes:
🔥 Oxidized LDL
🔥 High triglycerides
🔥 Low HDL
🔥 Small LDL particles
LDL is just a messenger. Insulin resistance loads the gun.
8. Your lipid panel is incomplete without these: Marker
Ideal Range
LDL-C < 100 mg/dL
HDL-C > 50 (F), > 40 (M)
Triglycerides < 100–120 mg/dL
ApoB < 80 mg/dL
Non-HDL-C < 130 mg/dL
TG:HDL Ratio < 2.0
📌 Always interpret in combination. One marker ≠ full story.
9. What really improves lipid profile?
And no, it’s not “eat less ghee.”
✅ Reduce seed oils & processed food
✅ Cut sugar, white flour, and excess rice/wheat
✅ Eat enough protein
✅ Lift weights
✅ Sleep well
✅ Correct insulin resistance
✅ Heal your gut
These fix LDL particles, not just numbers.
10. LDL often rises in low-carb or keto diets. Should you panic?
Not necessarily.
🔼 LDL rises
🔽 Triglycerides drop
🔼 HDL improves
🧪 ApoB stays normal
= Metabolic improvement overall
📍This pattern is called Lean Mass Hyper-Responder (LMHR) not high risk unless ApoB and inflammation rise.
11. Statins: Lifesaving or overprescribed?
✅ Beneficial for:
•Heart attack survivors
•Diabetics with high ApoB
•Genetic lipid disorders
⚠️ Not always necessary for:
Metabolically healthy people
Those with good ApoB, HDL, TG, CRP
Statins also lower CoQ10 and may increase diabetes risk in some.
Always ask: Risk vs Benefit.
12. Lp(a): The most ignored risk factor
Lip(a) is a genetically inherited LDL-like particle.
Highly atherogenic.
Normal LDL + high Lp(a) = still high risk.
🧪 Test once in lifetime.
❌ Not fixed by diet.
✔️ Controlled by niacin, diet, emerging therapies.
13. LDL is only a problem in a broken metabolic system.
A healthy person with:
✅ Low triglycerides
✅ High HDL
✅ Normal ApoB
✅ No inflammation
…can have “high” LDL and still be low risk
But a person with insulin resistance + high ApoB + inflammation = ticking time bomb even with normal LDL.
🔚 Final Truths:
🔸LDL is a messenger, not a villain
🔸Focus on ApoB, inflammation, insulin resistance
🔸Don’t treat numbers,treat the terrain
🔸Fix the system, not just the lab report
🔸Context is king
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Why are most Indian elders tired, bloated, or constipated?
It’s not age.
It’s nutrition.
ICMR’s dietary guidelines reveal how to fix this with food.
🧵 Diet plan for elderly people 👇 #ElderlyNutrition #ICMR
1️⃣ Energy Needs Decline, But Nutrient Needs Increase
With age, physical activity and basal metabolism slow down.
👉 Calories need to reduce by ~20% after 60 years
But nutrient density should increase.
Focus: small, frequent, nutrient-rich meals.
2️⃣ Protein Intake is Critical
ICMR-NIN recommends 1.0 g protein/kg body weight/day for elderly.
For a 60 kg elder, this means 60 g/day.
Essential for:
✔️ Preventing sarcopenia (muscle loss)
✔️ Immunity
✔️ Wound healing
My grocery for the week.
Protein-first. Real food.
It’s how obesity, diabetes, fatty liver & arthritis get reversed- from the kitchen, not the clinic.
Here’s how to build your diet from your cart 🛒 🧵👇
#ProteinPriority #MetabolicReversal
This is not a trend. It’s a system.
My cart reflects 4 goals:
✅ Fat loss
✅ Muscle retention
✅ Gut repair
✅ Inflammation control
The plan starts before the plate it starts at the store.
What I Bought And Why
🥚 Eggs – Best-quality protein, daily essential
🧀 Paneer – Slow-digesting protein, keeps me full
🥛 Milk – Turned into homemade curd = gut health + protein
🌿 Veggies & Greens – Fiber for digestion & sugar control
🍌🍈 Fruits – Seasonal & planned, not mindless
🥒 Okra & Kantola – Low-carb, anti-inflammatory
Type 2 Diabetes Is Reversible
Type 2 diabetes isn’t caused by sugar “ It’s caused by too much Belly Fat in your liver and pancreas.”
Prof. Roy Taylor proved it.
Obesity and diabetes are reversible,they’re not permanent life sentences.
Here’s how
Save & share this 🧵👇
1. Diabetes is not lifelong. It’s fat in the wrong places.
Prof. Roy Taylor’s research shows:
Type 2 diabetes happens when fat builds up inside the liver and pancreas, not just under your skin.
The solution? Remove this fat. Reverse the disease.
2. The Twin Cycle Hypothesis
🌀 Excess food → fat in liver
🌀 Liver becomes insulin resistant
🌀 More fat spills into pancreas
🌀 Pancreas stops making enough insulin
💩 Poop is one of the most powerful biomarkers in medicine but also the most ignored.
Each bowel movement reveals data on gut health, nutrient absorption, liver & pancreas function, inflammation, and immunity.
Here’s a scientific breakdown worth saving 🧵👇
#GutHealth
1️⃣ What exactly is poop made of?
On average:
🔸~75% water
🔸~25% solids
Of the solids:
🔸30% dead & living bacteria
🔸30% indigestible fiber
🔸10–20% fat
🔸10–20% inorganic matter
🔸Small amounts of protein, dead cells, bile pigments
This is microbial data, not just waste.
2️⃣ Color: A reflection of bile + liver function
🟤 Brown = Normal (from bile + bilirubin)
🟢 Green = Rapid transit, magnesium, leafy greens
⚫ Black = Upper GI bleeding, iron supplements
🔴 Red = Lower GI bleeding, hemorrhoids, fissures
🟡 Pale/Clay = Bile obstruction check liver
⚪ White = No bile. serious warning sign
Leptin: The Master Fat-Burning Hormone You’ve Never Heard Enough About
Struggling with weight loss even while eating less?
Always hungry even after meals?
The problem may not be willpower it may be Leptin Resistance.
Let’s dive deep 🧵 👇
#Obesity #Diabetes
What is Leptin?
Leptin is a hormone made by fat cells (adipocytes).
Its job is simple but powerful:
✅ Tells your brain: “You have enough energy stop eating.”
✅ Boosts metabolism
✅ Helps regulate fertility, immunity, and thyroid function
It’s often called the “satiety hormone” or “anti-starvation signal.”
How does Leptin work?
Leptin travels from fat tissue → to the brain (hypothalamus) and says:
🧠 “Energy levels are good. Reduce hunger. Burn more fat.”
So, more fat = more leptin = less hunger… in theory.
🫀 Key Cardiac Risk Markers You Shouldn’t Ignore
Heart attacks in 20s & 30s are becoming frighteningly common.
Fit on the outside ≠ Healthy on the inside.
Here’s how to investigate early & prevent silent cardiac risk 🧵 👇
🔴 1. Lipid Profile is just the beginning
Check more than just total cholesterol.
✅ LDL (bad cholesterol)
✅ HDL (good cholesterol)
✅ Triglycerides (TG)
✅ VLDL