What Marsha Eats

Coffee is not one drink. It is a category. The bean and water are constant across most home brewing, but the method changes which compounds end up in your cup. Two cups from the same bag can deliver very different chemistry depending on how they were brewed.

Four compounds matter for health. Caffeine drives the stimulant effect. Chlorogenic acids are the main polyphenols in coffee and carry most of its antioxidant activity. Diterpenes, specifically cafestol and kahweol, are oils that suppress the liver enzyme responsible for converting cholesterol into bile acids. When that enzyme slows, less cholesterol gets cleared and LDL goes up. Bitter phenolics accumulate with long extractions.

What the method controls. Angeloni et al. (Food Res Int 2020) compared eight brewing methods using the same beans. Espresso had the highest caffeine and polyphenol concentration per milliliter, three to six times more concentrated than drip or moka. But a shot of espresso is 30 mL. A cup of cold brew is 240 mL. Per cup, cold brew delivers more total caffeine and polyphenols because the serving is roughly eight times larger.

Diterpenes are where brewing method matters most for cardiovascular risk. They are oil-soluble, so a paper filter can physically trap them. Orrje et al. (NMCD 2025) measured these across methods. Paper-filtered drip: about 12 mg/L cafestol. French press and percolator: around 90 mg/L. Boiled coffee: 939 mg/L. Some espresso shots reached 2,447 mg/L, though espresso is highly variable. The paper filter is the key. Methods without one let the oils through.

This is why brewing method affects cholesterol. Jee et al. (Am J Epidemiol 2001) pooled fourteen randomized trials. Unfiltered coffee raised total and LDL cholesterol. Filtered coffee did not. Svatun et al. (Open Heart 2022, N=21,083) confirmed the signal in Norway. Drinking six or more cups of boiled or French press coffee daily was associated with total cholesterol about 9 to 12 mg/dL higher than non-drinkers. Filtered coffee showed only a small effect, mostly in women.

A note on the numbers. The per-cup mg values are estimates from per-mL concentrations times typical serving volumes. The relative ordering across methods is well-supported. Exact amounts depend on dose, grind, temperature, time, and bean. Espresso varies the most.

A note on cold brew. The graphic assumes paper filtration, which most commercial cold brew uses. Home cold brew through metal mesh or cheesecloth retains more oil and more diterpenes. The filter matters as much as the method.

The takeaway. If you want the caffeine and polyphenols without raising LDL, use paper-filtered methods. Espresso gives you concentrated chemistry in a small serving. French press and boiled coffee give you everything including the oils that raise LDL. Coffee is not one drink. The brewing method is the variable.

Choline is one of the few nutrients where the US population is genuinely under-consuming by intake. NHANES data show only 6.6% of US adults aged 19 and above meet the Adequate Intake (Wallace and Fulgoni, J Am Coll Nutr 2016). The shortfall is even larger in adolescents.

That matters because choline is not optional metabolism. It is the precursor for phosphatidylcholine (the major phospholipid in every cell membrane and the carrier that packages VLDL out of the liver), for the acetylcholine that runs cholinergic neurotransmission, and for betaine, a methyl donor that backstops the folate-dependent methylation system.

When you take choline out of human diets in controlled feeding studies, the consequences are not subtle. Fischer, da Costa et al. (Am J Clin Nutr 2007) fed 57 healthy adults a low-choline diet for up to 42 days. 77% of men and 80% of postmenopausal women developed fatty liver or muscle damage. Only 44% of premenopausal women did, because estrogen upregulates de novo phosphatidylcholine synthesis. Even at the current AI of 550 mg/day, six men in the study still developed organ dysfunction.

Niculescu et al. (Am J Clin Nutr 2007) showed that single-nucleotide polymorphisms in genes that interconvert choline, folate, and methyl pools modulate the requirement. People with variant alleles need more choline to avoid liver and muscle damage. The "AI" is a population average; individual requirement varies with genetics.

The food story is where the practical problem sits. Beef liver delivers 359 mg per 3-oz serving, but most people do not eat liver. Among foods people actually eat, one large egg at 147 mg is roughly twice the next-best common option (3 oz lean beef at 115 mg, salmon at 75 mg, chicken breast at 64 mg). Milk and most plant sources sit between 30 and 50 mg per serving. The math is not subtle: hitting 425 to 550 mg from non-egg foods alone requires deliberate planning around organ meats, fish, and legumes. Drop the eggs and the typical American diet falls well below the AI.

Two practical implications. First, the AI for choline is not aspirational. It is the dose calibrated against actual liver and muscle damage in controlled human feeding trials. Second, pregnant and lactating women have higher needs (450 and 550 mg/day) at a life stage where choline supports fetal brain development. The 2009-2012 NHANES data show pregnant women meeting the AI at rates similar to non-pregnant women, which is to say, rarely.

The "eggs are bad for cholesterol" advice removed the only convenient source of one of the few nutrients Americans actually run short on.

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Apple cider vinegar has built an entire wellness category on a real effect attributed to the wrong ingredient. The glucose-lowering data is genuine. The apple has nothing to do with it.

The acetic acid is what does the work, and any vinegar at the same concentration produces the same effect.

The original Johnston et al. study (Diabetes Care 2004) gave insulin-resistant and type 2 diabetic adults a vinegar drink before a meal containing 87 g of carbohydrates and saw postprandial glucose drop 64% in the insulin-resistant group and 19% in the diabetic group. The sample was small (n=29 crossover) but the effect size was large.

Ostman et al. (Eur J Clin Nutr 2005) ran the dose-response experiment. They served white bread with vinegar at three levels of acetic acid (18, 23, and 28 mmol) to healthy adults. Both glucose and insulin responses fell as acetic acid content rose. The effect tracked the acetic acid content, not the vinegar volume.

The 2017 meta-analysis by Shishehbor et al. (Diabetes Res Clin Pract) pooled the controlled trials. Vinegar consumption with a meal reduced postprandial glucose AUC (SMD -0.60, 95% CI -1.08 to -0.11) and insulin AUC (SMD -1.30, 95% CI -1.98 to -0.62). The effect is consistent and the magnitude is meaningful.

The mechanism is well-characterized. Liljeberg and Bjorck (Eur J Clin Nutr 1998) showed in healthy adults that adding vinegar to a starch meal delayed gastric emptying and that this delay tracked with the improved glycemic response. Slower emptying means slower carbohydrate delivery to the small intestine, which flattens the glucose curve. A secondary mechanism is inhibition of disaccharidase activity by acetate at the brush border. Neither depends on the source of the acetic acid.

The longer-term data is much weaker. Johnston et al. (Food Funct 2020) ran an 8-week trial of daily red wine vinegar in 45 adults at risk for metabolic complications. Fasting glucose and insulin sensitivity improved significantly, but body mass, waist circumference, and visceral fat did not change. The viral "ACV for weight loss" claim has thin support.

Two practical implications. First, if you want the postprandial effect, you need liquid vinegar at roughly 1 to 2 tablespoons. The dose has to deliver around 750 to 1500 mg of acetic acid. White, red wine, rice, and apple cider vinegars all work. Second, the gummies and tablets are a problem. Johnston et al. (J Nutr Metab 2022) tested commercial vinegar tablets head-to-head against liquid vinegar and found the tablets failed to lower postprandial glucose to the same degree.

The mother, the fermentation, the apple, the brand. None of it is the active ingredient. The acetic acid is.