On Astronomy - The Slow Theft of Time: Earth’s Rotational Energy, Tidal Friction, and the Fate of the Day

On Astronomy - The Slow Theft of Time:

Earth’s Rotational Energy, Tidal Friction, and the Fate of the Day

By blogger lim ju boo, alias lin ru wu (林 如 武) 

Post-doctoral - University of Oxford

 

Abstract

Earth’s rotation stores an immense reservoir of kinetic energy, accumulated since planetary formation. Yet this energy is not conserved within Earth itself: through tidal interactions with the Moon, a small but relentless fraction is dissipated as heat in the oceans and crust.

This article quantifies Earth’s rotational kinetic energy, estimates the rate at which it is lost to tidal friction, and explores the long-term dynamical consequence, namely the gradual lengthening of the day and Earth’s eventual tidal locking. Though imperceptible on human timescales, this process provides one of the most elegant examples of slow cosmic evolution governed by classical mechanics.

 

1. Rotational kinetic energy of the Earth

For a rotating rigid body,

K_rot = 1/2 Iω²

Where

I, is the moment of inertia and
ω (omega) is the angular velocity.

Earth parameters

Mass (M) = 5.972×10 ²⁴  kg  

(That's almost 6 followed by 24 zeros kg) 

Mean radius (R) = 6.371 × 10 ⁶ m

Angular velocity (sidereal rotation):

ω  = 7.292×10⁻⁵ rad s−1

Because Earth is centrally condensed, its measured moment of inertia is

I = 0.3307 MR²  ≈ 8.04×10³⁷ kg m²

Thus,

K_rot = 1/2 (8.04×10³⁷)(7.292×10⁻⁵)²​

 

≈2.1×10²⁹ joules​

(Those unfamiliar with mathematics, that means, 2 followed by a whopping, whooping 29 zeros joules of energy - I can't even dream that amount of energy the rotating Earth is endowed with by the Creator - can you?) 

This is the stored mechanical energy of Earth’s spin, independent of orbital motion or internal heat.

 

2. The mechanism of tidal energy loss

The Moon raises tidal bulges on Earth’s oceans and, to a lesser extent, its solid body. Because Earth rotates faster than the Moon orbits, these bulges are carried slightly ahead of the Earth–Moon line. The Moon’s gravity pulls backward on them, exerting a torque that:

1. Slows Earth’s rotation

2. Transfers angular momentum to the Moon

3. .Dissipates energy as heat via oceanic and crustal friction

This process obeys angular momentum conservation but not energy conservation, the “missing” energy is thermalised.

 

3. Measured rate of tidal dissipation

Geophysical measurements give the present tidal dissipation power as:

P_tides ≈ 3.7×10¹² w 

That is, 3.7 terawatts, comparable to human civilization total power consumption.

Energy lost per day:

E_day = P × 86400 ≈ 3.2×10¹⁷ Joules

Fraction of Earth’s rotational energy lost per day:

E _day / K _rot ≈ 3.2 x 10 ¹⁷ / 2.1 x 10 ²⁹ ≈ 1.5 x 10 ^{- 12}

That is:

0.00000000015% per day

 

 

4. Observable consequences today

Despite the tiny fraction, the effects are measurable:

Length of day increases by

~1.7 milliseconds per century

Moon recedes at ~ 3.8 cm per year

Ancient coral growth rings show ~ 400 days per year hundreds of millions of years ago. This confirms that the process has been active throughout geological history.

 

5. How long until Earth “comes to a halt”?

Strictly speaking, Earth will never stop rotating in an absolute sense.
Instead, it will approach a tidally locked state with the Moon.

Final configuration:

One Earth day = one lunar month

Earth always shows the same face to the Moon

No lunar tides (only solar tides remain)

Current estimates place this timescale at:

30–50 billion years.

This far exceeds the Sun’s remaining lifetime (~5 billion years).

Earth’s habitability window.

Even the Sun’s red-giant phase

Thus, Earth will be uninhabitable long before its rotation is exhausted.

 

6. A subtle but profound insight

Angular momentum is conserved.
Energy is not.

Earth’s lost rotational energy does not vanish:

It warms the oceans

It stirs currents

It fractures crustal rock

It drives geological evolution

Time itself, measured by the length of the day, is slowly forged by friction.

 

7.  The poetry of slow physics

Earth is not running down like a wound clock.
It is participating in a quiet celestial dialogue with the Moon.

Each tide whispers away an infinitesimal portion of spin,
stretching the day,
moving the Moon outward,
and reminding us that even the most stable rhythms of nature are temporary.

As the Moon continues its slow recession, the exquisite geometric coincidence that allows total solar eclipses will eventually be lost. The Moon’s apparent angular diameter will shrink below that of the Sun, and totality will give way forever to annular eclipses. Humanity happens to live in a brief cosmic window, a grace period measured in hundreds of millions of years, during which such perfection is possible.

That alone is a thought worthy of quiet reverence.

This is not decay. It is cosmic patience.

When Numbers Mislead: Atherosclerosis Progression, Mathematical Illusions, and Clinical Reality in the Elderly

 

窗体底端

 

Title: “When Numbers Mislead:

Atherosclerosis Progression, Mathematical Illusions, and Clinical Reality in the Elderly”

by this blogger -  lim ju boo, alias lin ru wu (林 如 武)

A close doctor friend of mine wrote this letter (in inverted comma) to me:

"Thank you very much Prof. Lim for your article here:

https://scientificlogic.blogspot.com/2026/01/can-atherosclerosis-and-stable-angina.html

 Very informative. For your information, my LDL was 80mg/dl, crp 3.5mg and the rest of the parameters were normal. Had a ECG & Stress Test and was normal. The cardiologist suggested a CT Angio in view of my age 78yrs. It took me 1 year to decide to do it after consulting 2 other cardiologists. It showed about 25% blockage. The cardiologist suggested only low dose Atorvastatin or Rosuvastatin and both caused muscle pain, so I stopped it after 10 days. I now restrict my vegan diet further. If LDL is still raised after one month, I may want to try Pravastin or Ezetimibe. Please advice and comment Prof Lim. Thanks".

 

Here is my answer for my beloved friend. 

 

Thank you doctor for your interesting question.  I thought instead of answering your question as an individual, I  should share out my answer and opinion to a much wider audience - without your name disclosed -  for general educational purpose, since coronary heart disease affects almost every one irrespective of age, and is the Number One Killer in most countries. It should  benefit everyone at risk who may be interested in reading my explanation. It took me some time to think over your question, analyze what you wrote, before I could write and answer here: 

Here are my opinion:

Atherosclerosis is commonly perceived as a progressive, age-dependent, and eventually obstructive disease. However, clinical observations, particularly in elderly individuals, often contradict this simplistic model. This article examines a real-world scenario of mild coronary atherosclerosis detected at an advanced age and explores, through a deliberately artificial mathematical extrapolation, why linear models of disease progression are fundamentally flawed. This discussion then reconciles mathematical intuition with biological reality, emphasizing plaque stability, inflammation, and clinical context over luminal narrowing alone. Therapeutic implications, particularly regarding lipid-lowering strategies in statin-intolerant elderly patients, are also addressed.

Let me Introduce this subject just a little bit more, although not 100 % complete yet. This will take me a longer time to answer and you may lose your patience with me. But I am very patient looking at the stars and galaxies which is my real hobby in astronomy - not all these medical stuff. 

Let me briefly answer:  

Coronary atherosclerosis is frequently framed, both in public discourse and in some clinical thinking, as a slow but relentless accumulation of plaque that inevitably worsens with age. This narrative encourages a numerical mindset: percentage stenosis, LDL targets, and chronological age are often interpreted as predictors of future obstruction and cardiovascular events.

Yet, daily clinical practice tells a more mixed story. Many elderly individuals harbour  coronary plaques that remain stable for decades, especially among vegans and stanched vegetarians,  while acute coronary syndromes often arise more among animal fat eaters and sugar consumers from lesions that were previously considered “non-significant.” This discrepancy invites deeper reflection on how we conceptualize disease progression.

Since I was a medical researcher with a love for mathematics and statistics, let me give my mathematical thought on experiment using linear progression (with age).

To illustrate the danger of oversimplification, consider this following hypothetical model.

Given the age of 78 years with coronary stenosis on CT angiography at 25%. Let us assume (intentionally unrealistic) that we have zero plaque at birth. Using statistical linear progression with age with no biological acceleration, regression, rupture, or healing, then this calculation would mean this:

Annual progression rate = 

 

25% / 78 years is approximately 0.32 % per year.

To reach 100% stenosis:

100 % / 0.32 % would approximately be 312 years. 

By then, we would have long died from other causes.

However, please note this result I present here is purely mathematical, and not biological. Under a purely linear, age-driven model, complete coronary occlusion would occur at approximately 300+ years of age.

This interpretation is absurd, I am afraid. Please note this result is purely mathematical based purely on a straight-line linear correlation, and is not biological as we age. This result is biologically impossible, and that is precisely the point.

The calculation exposes a fundamental truth in that atherosclerosis is not a linear function of time or age.

Age alone is a poor predictor of plaque behavior. The human arterial system is not a pipe that slowly fills with debris; it is a living, adaptive, inflammatory, and sometimes self-stabilizing organ.

The biological reality is,  how atherosclerosis actually behaves

Let me explain this in three steps:

 

1. Progression Is Non-Linear

Plaque accumulation occurs in fits and starts. Long periods of quiescence

Episodic acceleration during systemic inflammation, metabolic stress, infection, or oxidative injury. Possible stabilization or calcification over time. Many plaques stop progressing or become biologically inert - probably in your case at age 78?

2. Degree of Stenosis ≠ Cardiovascular Risk

Large clinical and pathological studies have shown that most myocardial infractions arise from plaques causing 30–50% stenosis, not severe obstruction as in your case.  The dominant determinant of risk is plaque vulnerability, not lumen narrowing

Key factors include, inflammatory activity, fibrous cap thickness and lipid core composition. Thus, a stable 25% lesion in an elderly individual may represent vascular success, not failure.

3. Imaging Shows Anatomy, Not Biology

CT coronary angiography provides valuable anatomical information on degree of luminal narrowing, calcification burden

However, it does not directly assess to inflammatory state, plaque stability and propensity for rupture. Clinical interpretation must therefore integrate imaging with functional testing, biomarkers, and symptoms.

The Central Role of Inflammation

In individuals with relatively low LDL levels, systemic inflammation becomes a dominant risk driver.

High-sensitivity C-reactive protein (hs-CRP) correlates strongly with cardiovascular events. Inflammation influences endothelial dysfunction, plaque destabilization, and thrombosis. In such cases, atherosclerosis behaves less like a lipid storage disease and more like a chronic inflammatory disorder.

Please read further my explanation on why the rate of atherosclerosis is not a linear progression, but an accelerated exponential scenario after middle age here: 

The Progression of Atherosclerosis and Coronary Heart Disease with Age

https://scientificlogic.blogspot.com/2026/01/the-progression-of-atherosclerosis-and.html

Let me now talk a little about  therapeutic implications in the elderly, namely statin intolerance - the question you asked and is worried about your  muscular pain. 

 We know that  statin-associated muscle symptoms are real, particularly in elderly patients, in individuals with low baseline LDL. Those with possible mitochondrial vulnerability. Discontinuation due to myalgia is clinically reasonable as in your case.

 

What then can we offer as alternative options for the elderly?  My answer is, Pravastatin - as you correctly suggested yourself as a doctor, because this  drug is hydrophilic with lower muscle penetration. It also has lower myopathy risk, and a modest LDL reduction

Ezetimibe has non-statin mechanism in pharmacological action. To the best of my knowledge its tolerability is excellent. However, it has limited benefit when LDL is already low

In patients with LDL of about  80 mg/dL, the absolute risk reduction from further LDL lowering is modest, and treatment should be individualized rather than target-driven.

Let me explain further

Thoughts on Pravastatin vs Ezetimibe - their challenges 

A. Pravastatin

Pros. It is hydrophilic, causing  less muscle penetration. It has lower myopathy risk, but a mild LDL reduction

Cons. It is still a statin. This drug may still provoke symptoms in sensitive individuals.  If tried, it should be low-dose and symptom-led, not target-led.

B. Ezetimibe

The pros is this drug is a non-statin. It acts at gut cholesterol absorption. It has minimal muscle side effects. It is well tolerated in elderly patients. The cons are, it has modest LDL lowering (~15–20%). It has limited effect if LDL is already low.  Given LDL = 80 mg/dL, the marginal benefit may be small, but tolerability is excellent.

 The deeper question: what actually stabilizes plaques?

From both evidence and physiology. Stability depends on inflammation control (CRP ↓). It also depends on oxidative stress reduction. It depends on endothelial function. Plaque stabilization is  not shrinkage

A vegan diet already addresses saturated fat, cholesterol intake. What remains are  modifiable targets, such insulin resistance (even in “normal” glucose), chronic low-grade inflammation. Sleep, stress, micronutrients (e.g. magnesium, omega-3 balance even in vegans)

Having explained all that, let me now re-frame  my earlier clinical question on total blockage once again because this is an important and misleading question. The key question is not:

“When will this patient reach 100% blockage?”

But rather, “Is the disease biologically active or clinically dangerous?”

In many elderly individuals like your good self, mild coronary atherosclerosis represents a stable, slow-burning process, like a charcoal fire, not an inevitable path to occlusion. It is not a petrol fire that suddenly burst into a big fire - I always like to give this analogy to doctors, scientists and patients alike. 

Mathematical extrapolation, when stripped of biological context, leads to misleading conclusions. Atherosclerosis does not obey simple linear rules, nor does age dictate destiny. In elderly patients with mild disease, normal functional testing, and low LDL levels, emphasis should shift from numerical obsession to plaque stability, inflammation control, and overall vascular health.

In such cases, the presence of modest plaque burden at advanced age may be interpreted not as impending catastrophe, but as evidence of remarkable physiological resilience.

I hope I manage to answer your question dear friend using  the best of my knowledge in medical research, in medicine, biochemistry, pharmacology, molecular biology and above all using my knowledge in medical nutrition which is the most important health-protective asset in preventive and curative medicine.

Let us all walk together in wisdom, not with acquired knowledge from universities or even through highly expensive and time honoured medical and scientific  research. 

I hope I have managed to answer  

References for Further Reading

1. Libby P. Inflammation in atherosclerosis. Nature. 2002;420:868–874.

2. Ridker PM et al. Inflammation, C-reactive protein, and cardiovascular risk. Circulation. 2003;107:363–369.

3. Naghavi M et al. From vulnerable plaque to vulnerable patient. Circulation. 2003;108:1664–1672.

4. Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:657–671.

5. Puri R et al. Impact of statins on plaque progression. J Am Coll Cardiol. 2015;65:1273–1285.

A Deadly Combination of Durian with Alcohol Consumption

My mother in the 1940’s used to tell me when I was only  a small child, never eat durians and drink alcohol at the same time or soon after that. She told me it will result in death.  I was then very small when she told me this.

Today, I am a clinician, a nutritionist, a retired senior medical researcher, but above all  - a medical and food toxicologist - formerly with the Massachusetts Institute of Technology working in collaboration with the Institute for Medical Research. I believe today I am in a much better position to speak on the scientific truth behind this traditional, social and cultural belief.

 

This deadly traditional belief has struck on for generations among most Malaysians. There were several reports I read in the newspaper and have also heard unconfirmed stories telling the same -  of deaths resulting from the consumption of durian together with alcohol. Especially currently in the peak durian season we need to be careful with what we eat.

 

This paper is meant for all healthcare professionals, including medical doctors who have no clue on this traditional belief.  Some doctors has even  dismissed it as an  “unscientific superstition”  

 

Title: Durian and Alcohol  -  Biochemical Evidence Supporting a Traditional Malaysian Dietary Prohibition

 

Abstract

 

For generations, Malaysians have been cautioned against consuming durian together with alcohol, with traditional warnings ranging from severe illness to sudden death. Often dismissed as folklore, this belief has persisted across cultures and decades. This paper examines the biochemical basis of this traditional prohibition by analyzing the metabolism of ethanol in the human body and the inhibitory effects of sulphur-containing compounds found in durian on key hepatic enzymes. Evidence suggests that durian can significantly impair aldehyde dehydrogenase activity, leading to toxic acetaldehyde accumulation. While the claim of inevitable fatality is exaggerated, the combination poses genuine physiological risks, particularly in individuals with underlying metabolic or cardiovascular disease. This work demonstrates how traditional dietary wisdom may align closely with modern biochemical understanding.

Introduction

Durian (Durio zibethinus), revered as the “King of Fruits” in Southeast Asia, is cherished for its distinctive aroma, rich taste, and high nutritional value. Alongside its popularity, however, exists a long-standing traditional warning: durian should never be consumed together with alcohol. This belief was widely known in Malaysia as early as the first half of the twentieth century and was often conveyed with grave seriousness, sometimes invoking the possibility of death.

With advances in biochemistry, toxicology, and nutritional science, it is now possible to examine whether this traditional belief has a physiological basis. To do so, one must first understand the normal metabolic fate of ethanol in the human body.

Ethanol Metabolism: A Biochemical Overview

Absorption and Hepatic Processing

Ethanol is rapidly absorbed from the gastrointestinal tract into the bloodstream and transported to the liver, which serves as the primary organ for its metabolism. The detoxification of ethanol occurs via a tightly regulated two-step enzymatic pathway involving:

Alcohol dehydrogenase (ADH)  and  Aldehyde dehydrogenase (ALDH)

This system normally prevents the accumulation of toxic intermediates.

Step 1: Ethanol to Acetaldehyde (Alcohol Dehydrogenase)

The first step occurs in the cytoplasm of hepatocytes, where alcohol dehydrogenase (ADH) catalyzes the oxidation of ethanol into acetaldehyde:

Ethanol + NAD⁺ → Acetaldehyde + NADH + H⁺

Acetaldehyde is a highly toxic and carcinogenic compound, far more harmful than ethanol itself. It is responsible for many acute alcohol-related symptoms, including facial flushing, nausea, headache, tachycardia, and tissue injury. Therefore, rapid removal of acetaldehyde is essential for physiological safety.

Step 2: Acetaldehyde to Acetate (Aldehyde Dehydrogenase)

Acetaldehyde is promptly transported into the mitochondria, where aldehyde dehydrogenase (ALDH), particularly the mitochondrial isoenzyme ALDH2, oxidizes it into acetate:

Acetaldehyde + NAD⁺ + H₂O → Acetate + NADH + H⁺

This step is normally highly efficient, ensuring that circulating acetaldehyde levels remain extremely low.

Final Metabolic Fate

Acetate is relatively non-toxic and exits the liver to circulate to peripheral tissues such as muscle and brain. There, it is converted into acetyl-CoA, enters the citric acid (Krebs) cycle, and is fully oxidized to carbon dioxide and water, generating metabolic energy in the form of ATP.

In summary, under normal conditions: ADH initiates ethanol metabolism. ALDH completes detoxification. Toxic intermediates do not accumulate.

ADH and ALDH: Distinct but Complementary Roles

Although ADH and ALDH function sequentially, their physiological roles differ profoundly. Alcohol dehydrogenase (ADH) converts ethanol into acetaldehyde
Cytoplasmic localization produces a highly toxic intermediate . Aldehyde dehydrogenase (ALDH) converts acetaldehyde into acetate
ALDH2 is predominantly mitochondrial. Detoxifies aldehydes and protects tissues

ALDH enzymes form a family of NAD(P)+-dependent enzymes responsible for oxidising a wide range of toxic endogenous and exogenous aldehydes. ALDH2 deficiency or inhibition leads to acetaldehyde accumulation, manifesting clinically as the alcohol flush reaction.

Crucially, ADH activity often exceeds that of ALDH. Therefore, any impairment of ALDH function rapidly results in acetaldehyde buildup and systemic toxicity.

Durian and Enzyme Inhibition

Sulphur Compounds in Durian

Durian contains several volatile sulfur-containing compounds responsible for its characteristic aroma. Among these, diethyl disulfide has been shown to significantly inhibit aldehyde dehydrogenase activity.

Experimental studies, including those from the University of Tsukuba (Japan), demonstrate that diethyl disulfide can reduce ALDH (particularly ALDH2) activity by up to 60–70%.

Biochemical Consequences of Co-Consumption

When alcohol is consumed together with durian. ADH continues to convert ethanol into acetaldehyde. ALDH activity is inhibited by durian sulfur compounds. Acetaldehyde like formaldehyde  accumulates rapidly in the bloodstream and may even cause blindness. Other results in symptoms resembling severe alcohol intolerance like,  intense facial flushing, severe nausea and vomiting, dizziness and headache, palpitations and chest discomfort and profound malaise and distress

Additional Metabolic and Cardiovascular Stress

Durian is also high in natural sugars, calorically dense, and capable of transiently increasing blood pressure and heart rate

Alcohol contributes further physiological strain through vasodilation, dehydration, and sympathetic activation. In individuals with diabetes mellitus, hypertension, coronary artery disease, or cardiac arrhythmias, this combined metabolic burden may precipitate serious adverse events, including hypertensive crises, arrhythmias, or myocardial ischemia.

This provides a plausible explanation for rare but credible reports of collapse or death following durian–alcohol co-consumption.

Discussion: Tradition Anticipating Science

The traditional Malaysian warning against consuming durian with alcohol is not merely cultural superstition. While claims of inevitable or immediate death are exaggerated, modern biochemistry clearly demonstrates that the combination is physiologically hazardous, particularly in vulnerable individuals.

This case exemplifies how empirical cultural wisdom, transmitted across generations, can precede and is in line in the same frequency with scientific discovery.

The consumption of durian together with alcohol disrupts normal ethanol metabolism by inhibiting aldehyde dehydrogenase, leading to toxic acetaldehyde accumulation. While not universally fatal, the combination can cause severe adverse reactions and may be dangerous in individuals with underlying medical conditions.

Accordingly, avoidance of alcohol for several hours before or after durian consumption is strongly advisable. In this instance, traditional dietary guidance stands validated by modern biochemical science.

Selected References

1. Zakhari, S. (2006). Overview: How is alcohol metabolized by the body? Alcohol Research & Health, 29(4), 245–254.

2. Edenberg, H. J. (2007). The genetics of alcohol metabolism. Alcohol Research & Health, 30(1), 5–13.

3. Yokoyama, A., et al. (2010). Alcohol flushing, alcohol and aldehyde dehydrogenase genotypes, and risk for esophageal cancer. Alcohol, 44(2), 123–130.

4. Maninang, J. S., et al. (2009). Inhibition of aldehyde dehydrogenase by sulfur compounds in durian. Journal of Agricultural and Food Chemistry, 57(21), 10342–10347.

5. Lieber, C. S. (1997). Ethanol metabolism, cirrhosis and alcoholism. Clinical Chimica Acta, 257(1), 59–84.

 

1. thanol + NAD