Phosphatidylethanolamine N-methyltransferase
PEMT is an enzyme in the liver that converts phosphatidylethanolamine (PE) into phosphatidylcholine (PC) using methyl groups. PC is not a “nice to have.” It is structurally essential.
What PEMT does
Without adequate PC, three foundations begin to falter:
Bile becomes thick and sluggish. PC makes up 40–60% of bile’s emulsifying structure. When PEMT is compromised, bile carries less phosphatidylcholine, making it more acidic and more detergent-like. This irritates mucosa, increases inflammation, and reduces bile’s ability to bind and escort fats, hormones, heavy metals, and fat-soluble toxins out of the body.
Cell membranes lose resilience. The fluidity and flexibility of every cell membrane depends on PC. Low PEMT activity leads to membranes that are more rigid, inflamed, and prone to leakage. Clinically, this can look like bloating, poor fat digestion, reactive hypoglycaemia, neurological dysregulation, and difficulty tolerating oestrogen shifts.
Hormones cannot be cleared efficiently. PC is required for the formation and flow of bile, and bile is one of the major pathways for oestrogen disposal. Low PEMT means low PC, which means slow bile, which means oestrogen recirculates. This is a key driver of oestrogen dominance, breast tenderness, heavy cycles, histamine sensitivity, and inflammatory water retention.
The TT genotype
The TT genotype reduces PEMT efficiency significantly. Research shows that individuals with TT often cannot produce enough phosphatidylcholine endogenously, especially under stress, inflammation, or increased hormonal load. They rely heavily on dietary choline to compensate. When intake is insufficient, the system compensates by pulling PC from its structural role in cell membranes and liver tissue. Over time this is associated with NAFLD, gallbladder issues, IBS-like symptoms, chronic fatigue, and a feeling of “sluggishness” despite a healthy diet.
Symptoms and patterns to look for
- Lifelong tendency towards fluid retention
- Sensitivity to oestrogen shifts
- Sluggish bile flow and bloating when fat intake increases
- Difficulty metabolising fat without targeted support
- Lipedema-like presentations (poor lymph flow overlaps strongly with poor bile flow)
- Noticeable benefit from lecithin intake
- Immediate energy improvement from choline-rich foods (egg yolks, salmon, anchovies, liver)
Food support for PEMT TT
Because the enzyme is intrinsically inefficient, the system needs daily choline rather than sporadic intake. Supportive foods include:
- Egg yolks
- Organic liver (or desiccated liver)
- Sunflower lecithin (1–2 tsp daily, split AM/PM if needed)
- Salmon, sardines, and anchovies
- Brussels sprouts, broccoli, cabbage (mild choline contribution plus sulphur support for oestrogen clearance)
- Fermented foods (modulates bile–microbiome cross-talk)
Nutritionists will prescribe a combination of lecithin, methylated B vitamins, and sulphur-rich vegetables tends to produce the strongest response in TT carriers. WE use high quality food and ingredients to support this and fermentation on the proven bread.
Clinical consequences if unaddressed
In TT carriers, unaddressed PEMT disruption is strongly linked to poor bile flow, steatosis/fatty liver risk, oestrogen dominance and recirculation, histamine intolerance due to mucosal fragility, gallbladder issues, slowed detoxification of fat-soluble toxins, cognitive fatigue, and poor metabolic flexibility.
These tendencies are amplified when PEMT TT intersects with other variants such as MTHFR (reduced methylationefficiency), COMT (slower oestrogen metabolism), GSTM1 null (reduced glutathione), and ABCB1 (reduced cellular efflux of conjugated toxins).
How it connects to BALM
PEMT is one of the core nutrigenetic drivers for why botanical diversity, fermentation, and choline-rich food structures matter within the BALM framework. This is explored further in Why bread is the perfect medium to deliver both choline and methylated folate.
- Fermentation liberates B-vitamins and methyl donors that support the methylation side of PEMT
- The Botanical Blend increases fibre viscosity and supports microbial species such as Akkermansia, which help maintain mucosal integrity compromised by poor bile acids
- The fat–fibre structure of Diversity Bread slows absorption, stabilises blood sugar, and reduces inflammatory load on the liver
This is a brilliant example of how a single SNP radiates outwards across multiple BALM principles—bile flow, fermentation, diversity, fat metabolism, emotional regulation, and hormonal stability.
A personal note
I am PEMT TT myself. For years I experienced fluid retention, sensitivity to hormonal shifts, and bloating when my fat intake increased—without understanding why. When I finally had my genetics tested, PEMT explained a pattern I had been living with my whole life.
What I notice now: better digestion, improved drainage, and reduced inflammation when my PC intake is high. Lecithin, methylated B vitamins, and sulphur-rich vegetables make an immediate difference to my energy. Even reducing carotenoids has helped—fewer fat-soluble molecules to process through sluggish bile.
My genetics also include MTHFR AG, COMT AG, GSTM1 null, and ABCB1 AA, which means PEMT sits at the centre of a much larger picture. Understanding this changed how I eat, how I bake, and how I teach.
