A few months ago I was having a conversation with a group of friends — all desis, all in their late thirties and early forties, all reasonably health-conscious. One had joint pain that hadn’t resolved despite months of physiotherapy. One was constantly fatigued despite sleeping enough. One had been told by his doctor that his hs-CRP was “a little elevated” but not to worry about it.
The word that kept coming up was inflammation.
None of them had been given a clear explanation of what that actually meant, where it was coming from, or what to do about it. They had been handed the result and sent on their way.
I recognised the pattern immediately. Not because I had studied it academically — but because I had lived it, and then spent two years understanding it and doing something about it.
What inflammation actually is
Before we get into the desi-specific piece, let me be precise about the term, because it gets used loosely in ways that create more confusion than clarity.
Inflammation is your immune system’s first-response mechanism. When you cut your finger, the redness, warmth, and swelling around the wound is inflammation doing exactly what it is supposed to do: rushing blood and immune cells to the site, cleaning up damaged tissue, and beginning repair. This is acute inflammation. It is essential and protective.
The problem is a different kind: chronic low-grade inflammation. No wound. No infection. Just a persistent, low-level immune activation that runs in the background for months or years, silently driving damage to blood vessels, impairing insulin signalling, degrading muscle and joint tissue, and accelerating biological aging.
This is what my friends were describing. And it is what the research consistently shows is disproportionately common in South Asian populations — often without obvious symptoms until it is already causing downstream problems.
The genetics twist: my report said I was fine
When I got my 3×4 Genetics report back, I went straight to the inflammation section.
The result: LOW impact. My TNFA variants — the genes associated with TNF-alpha, one of the primary pro-inflammatory cytokines — were both GG. No elevated risk. My IL-6 gene came back GG as well. Normal. My CRP gene variant, which influences baseline C-reactive protein production, was present but not in the high-impact category.
On paper, I am not genetically predisposed to chronic inflammation. The system looked at my DNA and said: this pathway is not your primary concern.
And yet, when I tested my hs-CRP about two years ago, it came back at 2.4 mg/L. That is above the optimal threshold. Not dangerously high — but sitting in a zone that tells you something is running in the background that should not be.
This is the most important thing I can tell you about inflammation: genetics sets your baseline tendency, but lifestyle determines the outcome. Low genetic risk does not protect you from chronic inflammation if your diet, sleep, and training are driving it up. And the reverse is also true — high genetic risk can be significantly modulated by the right interventions.
My genetics gave me a favourable hand. I had partially squandered it. Then I fixed it.
You’re not bloated. You’re inflamed.
There is a phrase I hear a lot from desi friends and family: I just feel bloated all the time. Puffy. Heavy. Sluggish after meals. Joint stiffness in the morning. A low-level tiredness that sleep does not fully fix.
Most of the time, this is not a digestion problem. It is inflammation — specifically the chronic low-grade kind that desis carry at disproportionately high rates, often without knowing it.
There are structural reasons why South Asians tend to carry higher inflammatory burden, even when the genetic predisposition is not there.
Visceral fat is the primary driver. Desis store fat differently from Western populations. We accumulate visceral fat — the deep abdominal fat that wraps around organs — at lower overall body weights and lower BMIs than comparable non-South Asian individuals. Visceral fat is not passive storage. It is metabolically active tissue that secretes pro-inflammatory compounds called adipokines continuously. The more visceral fat present, the higher the inflammatory load. You do not need to look overweight for this to be happening in your body.
The modern desi diet is quietly inflammatory. The food our grandparents ate in India — dal, sabzi, whole grains, fresh curd, turmeric in everything — was genuinely anti-inflammatory. What many of us actually eat in the US is a different story: packaged snacks with refined seed oils, maida in most restaurant food, late dinners that spike glucose before sleep, almost no omega-3s. The spice cabinet has been replaced by the snack drawer.
Sleep debt compounds everything. Chronically poor sleep — not terrible sleep, just consistently getting six hours instead of seven-and-a-half, going to bed at different times, being on your phone until midnight — elevates inflammatory markers measurably. hs-CRP in particular is highly responsive to sleep quality. I have seen this in my own data.
My genetics report actually flagged this indirectly. While my direct inflammation pathway was rated low, my Oxidative Stress pathway came back HIGH. The GPX1 gene (which codes for an enzyme that neutralises free radicals) showed a variant associated with reduced antioxidant capacity. The MNSOD gene, another key antioxidant enzyme, also showed impact. Oxidative stress and inflammation are not the same thing, but they are tightly coupled — chronic oxidative stress sustains and amplifies inflammatory pathways. A low inflammation genetic risk with a high oxidative stress profile is not a clean bill of health. It is a conditional one.
What I measured and what it showed
The key marker for systemic inflammation is hs-CRP (high-sensitivity C-reactive protein). This is the test I track and the one I recommend every desi ask for at their annual physical.
Your liver produces CRP in response to inflammatory signals anywhere in the body. The high-sensitivity version of the test can detect low-level chronic inflammation that the standard CRP test misses.
*Targets:*
- Below 1.0 mg/L — optimal
- 1.0–2.0 mg/L — acceptable
- Above 3.0 mg/L — elevated risk
My reading two years ago: 2.4 mg/L. Above optimal. Not a crisis, but a clear signal that something was running that should not be.
My reading now: 0.5 mg/L. Low end of excellent.
Same genetics. Different lifestyle. That is the entire point.
What I changed — and what actually moved the needle
I want to be specific here, because vague advice like “eat anti-inflammatory foods” is not useful. These are the actual interventions, in rough order of impact based on what I observed.
*1. Sleep consistency, not just duration*
The single most impactful change was not what I ate or how I trained. It was fixing my sleep timing. I was already sleeping around seven hours most nights. What changed was consistency: same wake time every day, including weekends. Reducing screens in the hour before bed. Keeping the bedroom cooler and darker.
I track sleep on my Oura ring. Within three weeks of consistent sleep timing, my resting heart rate dropped and my HRV improved. The inflammatory effect of sleep is largely driven by circadian rhythm disruption — your body’s repair processes run on a clock, and late irregular sleep is like a factory shutting down the maintenance crew before they finish the job.
*2. Removing ultra-processed foods entirely*
Not reducing. Removing. Packaged snacks, seed oil-heavy takeout, anything with a long ingredient list of things I could not pronounce. The mechanism here is straightforward: refined seed oils (corn, soybean, canola) are high in omega-6 fatty acids. At the ratios most people consume them — heavily dominant over omega-3s — they feed the inflammatory cascade directly. Traditional Indian cooking used ghee, mustard oil, and coconut oil. The move to “heart healthy” vegetable oils was arguably not an upgrade for inflammation.
*3. Reducing refined carbohydrates, not all carbohydrates*
I did not cut carbs dramatically. I removed the specific refined carbs that drive glucose spikes: maida products, white bread, biscuits, highly processed rice dishes. I kept dal, whole vegetables, some brown rice and millets. The distinction matters — glucose spikes drive insulin spikes, and chronically elevated insulin promotes inflammatory signalling. You do not need to go low-carb. You need to go low-spike.
*4. Adding anti-inflammatory foods deliberately*
This is where the desi kitchen is genuinely your advantage, if you use it properly.
I start every morning the same way, before coffee or food: 12 oz of warm water, freshly grated ginger, a squeeze of lime, a dash of cayenne pepper, and a shot of BEAM electrolytes. It is a small ritual but it does several things at once — it hydrates before anything else goes in, the ginger and cayenne both have well-documented anti-inflammatory effects, and the lime provides vitamin C, which my genetics flagged as a higher-than-average requirement. It takes about two minutes and it sets the tone for the rest of the morning.
Beyond that: turmeric with black pepper is now a daily habit, not an occasional one. The piperine in black pepper increases curcumin absorption by up to 20 times — haldi alone does very little in isolation. I add the combination to salads, a quick pickle on the side of a meal, or blended into a smoothie. Ginger in cooking and chai. Omega-3 supplementation daily — I do not eat fish, so I supplement directly rather than rely on dietary sources. Flaxseeds added to breakfast. Dark leafy greens daily.
This is not exotic or expensive. It is how Indian food was largely eaten before we started optimising for convenience.
*5. Shifting training: less volume, higher load*
I was training hard but with too much volume — multiple sets, frequent sessions, inadequate recovery between them. High-volume training at moderate intensity is a sustained inflammatory stimulus. The body needs to mount an inflammatory response to repair muscle damage after every session. If sessions are too frequent and volume is too high, that inflammatory load never fully resolves before the next one starts.
Moving to higher load with lower volume — fewer sets, heavier weights, more recovery between sessions — produced the same or better strength outcomes with significantly less inflammatory burden. This is consistent with what the research shows: it is chronic excessive training volume, not intensity, that drives systemic inflammation in recreational athletes.
My genetics actually supports this. My Recovery pathway came back HIGH, meaning I need more recovery time between training sessions than average. I had been ignoring this by training too frequently.
What to ask your doctor
If you take nothing else from this, take this: get your hs-CRP tested at your next blood draw. It costs almost nothing. It is not routinely ordered. Ask for it specifically.
Optimal is below 1.0 mg/L. If yours is above 2.0, you have a clear intervention target. If it is above 3.0, treat it as a priority and work with your doctor on the drivers.
For a fuller picture, pair it with the markers from my previous post — fasting insulin, ApoB, and the triglyceride-to-HDL ratio. Together, these give you a metabolic picture that the standard panel simply does not provide.
The bigger point
My genetics told me I was not particularly prone to chronic inflammation. That was never an excuse to ignore it.
Desi professionals in the US are, on average, eating a diet that promotes inflammation, sleeping inconsistently, overtraining on volume and under-recovering, and not measuring any of it. The genetic starting point matters less than the environment you build around it.
The good news — and this is the genuine good news — is that hs-CRP is one of the most responsive markers I track. The changes I described above moved mine from 2.4 to 0.5 in roughly four months. That is not a medical treatment. It is eating differently, sleeping on a schedule, and training smarter.
Your body is telling you something. The test is just how you listen.
If you have not already, read my post on the five lab markers every desi should test — including how hs-CRP fits into the broader picture of metabolic health.
