Low methylation potential leads to hypermethylation of genes

One would think that low methylation potential should result in hypomethylation of genes, but no, quite the opposite.

The paper below found that low methylation potential resulted in hypermethylation of FADS2.

Our findings demonstrate that the reduced methylation capacity in mice with HHcy is associated with hypermethylation of Fads2, lower Fads2 mRNA, and lower Δ(6)-desaturase activity in liver.

We also found higher PE/PC ratios in liver, primarily due to higher levels of PE with little changes in PC, and lower levels of PEMT activity in mice with HHcy.

This was accompanied by higher levels of 18:2n-6 and 18:3n-3 and lower levels of 20:4n-6 and 22:6n-3 in liver PC, and higher levels of 18:2n-6 and lower levels of 20:4n-6 in liver PE.

These findings suggest that the reduced hepatic methylation capacity in HHcy is associated with methylation silencing of Fads2 expression resulting in impaired synthesis of long chain polyunsaturated fatty acids and elevation of PE due to reduced synthesis of PC via the PEMT pathway. (R1)

If the same is true for humans, then we should expect reduced transformation of essential fatty acids (Linoleic and alpha-linolenic) into ARA, EPA and DHA when methylation potential is low.
Which means unhealthy phospholipid composition in the cellular membranes.