On nicotine, the brain, and the cost of a five-rupee pouch
In part 1 of this article, I have spoken at length about this story. Read it here
After the third recurrence, I very curiously asked, “Why did you continue chewing tobacco?”
And the painter answered without hesitation. “It kills hunger, madam. If I chew, I can work longer and save money on lunch.”
And the science, quietly agrees with him… Let me explain.
The answer is in the hypothalamus.
The hypothalamus is the brain’s oldest hunger regulator. It does nothing else except listen to the gut, to fat tissue, to the bloodstream, to a continuous conversation of hormones and neuropeptides that rise and fall with every meal, every hour of fasting, every demand the body places on itself. It collects all of that information and produces a single answer: eat, or do not eat.
When it says eat, the body feels hungry. When it says stop, the urgency passes.
This is not conscious. It is the body’s most fundamental act of self-preservation.
Nicotine, absorbed through the oral mucosa within minutes of the tobacco being placed in the mouth, crosses into the bloodstream and reaches this region of the brain rapidly. There, it binds to nicotinic acetylcholine receptors (nAChRs ) structures present throughout the hypothalamus, well positioned to play a central role in appetite and energy regulation. What follows is not a single event. It is a cascade that dismantles, one by one, almost every signal the body uses to say that it is hungry.
The first target is Neuropeptide Y (NPY). NPY is the brain’s most urgent hunger signal. It rises during fasting, floods the arcuate nucleus during starvation, and drives the body toward food with a force that is almost impossible to ignore under normal circumstances. Nicotine silences it. Studies show that acute nicotine administration reduces NPY concentration in the hypothalamus , a 33% fall in the arcuate nucleus and a 40% reduction in NPY messenger RNA within days of use. The hunger alarm is not merely quieted. It is chemically dismantled.
Alongside NPY sits its counterpart POMC, pro-opiomelanocortin. Where NPY drives the body to eat, POMC tells it to stop. Nicotine activates POMC neurons directly. In an experiment, animals in which POMC neurons were genetically removed showed no reduction in food intake when given nicotine confirming that this pathway is not incidental but essential. Nicotine effectively tips the balance between the brain’s hunger-drive and its satiety-drive, suppressing one and amplifying the other at the same time.
No food has been eaten. The stomach is empty. The blood glucose is unchanged. The man pressing khaini against his gum has been working for three hours in the heat and has consumed nothing. But the brain has been reorganised, in its own molecular language, to say that eating is not necessary.
It does not stop there.
Nicotine also stimulates the release of norepinephrine , a catecholamine both inside and outside the hypothalamus. The paraventricular nucleus of the hypothalamus contains receptors that, when activated by norepinephrine, directly suppress food intake. In animal studies, lesions that reduced norepinephrine levels in this region completely blunted nicotine’s ability to reduce meal size,demonstrating that this pathway is not theoretical but functional. The same fight-or-flight chemistry that prepares the body for danger also, in the presence of nicotine, tells the body it has no need for food.
Then there is leptin the hormone that fat tissue releases to signal that energy reserves are sufficient. When fat stores fall, leptin falls, and hunger rises. Nicotine appears to increase the brain’s sensitivity to leptin upregulating leptin receptors in the hypothalamus so that even a malnourished body reads its own depleted reserves as adequate. The body is running out. It is being told it is not.
And beyond the brain, nicotine acts on the gut directly. It activates sympathetic outflow to the liver, fat tissue, and gastrointestinal tract. It suppresses the visceral signals that travel up the vagal nerve to inform the brainstem that the stomach is empty. Studies confirm that food intake decreases in a dose-dependent manner with rising nicotine levels meaning the more tobacco, the more complete the suppression. Subjective hunger ratings fall by nearly 18% after nicotine administration, while those given a placebo report hunger rising. The body that has not eaten is not made to feel it has not eaten. That is the pharmacology in its plainest form.
The hunger is not gone. The body still needs food needs glucose, protein, iron, every micronutrient that the skipped lunch would have delivered. But every system designed to say so has been overridden, at multiple levels simultaneously, for the cost of five rupees.
This is what the painter discovered on a scaffolding over years of labour.
The hunger was not gone. Only the feeling of it was.
The research on manual workers in India places this pharmacology inside a human context that is impossible to look away from.
A study of 1,200 municipal solid waste management workers found that 71.5% were current smokeless tobacco users . Across construction workers, public transport workers, mine workers, and daily wage labourers, studies document smokeless tobacco prevalence between 60 and 91%. These numbers describe a pattern of where the hardest physical labour happens, where the body is most relentlessly demanded of, and where the gap between physical output and nutritional intake is widest.
Smokeless tobacco use is closely associated with the type of physical and mental stress a person carries in their work. Those who endure the most sustained physical effort ,who lift heavy loads, work in demanding environments, remain on their feet for long hours are the highest consumers. This is not a moral failure on anyone’s part. It is a physiological response to an unmet need, emerging quietly at the intersection of labour, hunger, and the body’s own chemistry.
The body, meanwhile, is keeping a different account.
While the brain is being told it is not hungry, the body is running a slow and cumulative deficit. India’s National Family Health Survey-5, covering over 795,000 participants, found that after adjusting for all sociodemographic factors, smokeless tobacco users had the highest proportion of underweight adults of any tobacco category. The BMI-lowering effect of tobacco in India is more pronounced for smokeless forms than for smoked ones.
The depletion does not stop at body weight. Smokeless tobacco has been consistently associated with iron deficiency anaemia in both men and women. It alters the sense of taste, making food less rewarding and appetite harder to sustain. It quietly redirects household spending away from nutrition .
The tobacco suppresses the hunger. The tobacco also consumes the money that could have fed the hunger. Both at once. In the same body. From the same pouch.
The intervention most likely to succeed is the one that understands the original problem. The one that meets the person where the habit began — not just where the disease finally arrived. – Wait for Part 3 of this….