An original introduction to the science and nutrition of apple cider vinegar (ACV) supplementation for horses
Or; fact versus fantasy
ACV is a popular supplement given to horses (as well as cattle and people), and has been claimed to do everything from curing cancer to osteoporosis, to repelling mosquitos.
This is the first comprehensive introduction into the known science of ACV for the use of regulating energy in the horse. It will be shown that the majority of ACV’s benefits for energy regulation are due to its ingredient acetic acid. It will also be shown that acetic acid is absorbed through the stomach, whereupon it enters the bloodstream, interacting with a range of tissue types. The roles for the liver, pancreas, skeletal muscle, intestines and their microbiota will all be discussed.
Contents:
- Preface
- Vinegar-acetic acid-acetate chemistry
- Insulin, glucose, and IR
- Acetic acid biology
- Acetic acid and IR
- Acetic acid cell signalling
- Appendix: Justifying heterozoonotic comparisons
- Conclusions and further research
1. Preface:
I believe that ACV can benefit energy regulation in reducing the risk of IR, and for reducing the risks associated with energy dysregulation in IR horses. ACV pharmacology mimics the upstream activation of known diabetes-2 drugs, including metformin.
I believe that the actions of ACV are predominantly due to acetic acid and that acetic acid is rapidly absorbed upon ingestion whereupon it activates receptors that control insulin release and sensitivity, glucose transport and metabolism, lipid metabolism, gut motility, and possibly gut microbiota. Most effects are due to immediate actions of acetic acid at cell membranes, although some effect likely depends on acetic acid uptake into cells, or gene expression, or microbiota.
I believe that ACV (qua acetic acid) is one of the best and safest regulators of equine (and human) energy metabolism, and recommend that every individual consider whether ACV could benefit their horse.
There is very little evidence on ACV in horses. Most of the following depend on non-ACV vinegar (which is easily justified), and on non-equine studies. For those who question that latter assumption, I advise immediate perusal of the appendix.
2. Vinegar-acetic acid-acetate chemistry:
Vinegar has been traditionally produced by fermentation of alcohol. This involves the microbial conversion of ethanol (alcohol, CH3CH2OH) in the presence of oxygen into acetic acid (CH3COOH). Acetic acid is the second major ingredient of vinegar after water.
Acetic acid is considered to be a weak acid. This means that it will donate hydrogen ions under appropriate conditions, but less than a strong acid like hydrochloric acid.
Acetic acid is the same as acetate, albeit depending on whether it is existing as a salt or proton donor, and depends predominantly on the pH of the chemical environment.
The terms “acetic acid” and “acetate” are used here interchangeably. Note however that consumption of an acetate salt (e.g. sodium acetate) does not have the same effect on metabolism
4. General acetic acid biology:
Acetic acid is one of the main by-products of microbial fibre fermentation in the hindgut. It is the simplest and shortest of the SCFA (short chain fatty acids, also including butyrate and propionate).
SCFA are absorbed into the gut wall through some combination of hydrogen, sodium, carbonate exchange and passive diffusion.
SCFAs are packaged into triglycerides by the liver, although acetate is not the preferred substrate, and can be preferentially used in its original state. Acetate is a single modification away from being used by the Krebs Cycle, which is a series of biochemical reaction used to produce cellular energy (in the form of a molecule called ATP, adenosine triphosphate, and its derivatives ADP, AMP, cAMP).
Acetic acid ingestion and digestion:
Acetic acid can cross the gastric and intestinal wall down a concentration gradient, exchanged by carbonate, which could explain its ability to increase gastric (stomach) pH. Any changes to gastric or enteric (gut) pH are expected to be rapidly buffered; forcing the gut to readjust its pH and possibly rescuing dysfunctional pH states.
There has been research into vinegar’s effects on stomach mucus, with suggestions that there can be short-term weakening (permeability) of the mucosa, but this is compensated within a few days. The safety of vinegar for pre-existing ulcers is difficult to definitively argue. Most of the research into acetic acid and ulcers or cancer should be carefully perused, due to the intended and artificial use of high concentrate and extended exposure.
Following gastric (stomach) absorption, the acetic acid can be rapidly detected in the blood. Questions have been raised regarding the role of gastric pH and delayed gastric emptying as mechanisms of action for acetate. Acetate can induce a release of the enteric hormone GRP1 by L-cells, which act at GRP1R (receptor) to delay gastric emptying.
6. Acetic acid cell signalling:
Acetic acid is known to activate a number of cell signalling pathways, although the degree of interaction or interdependence between these pathways remains to be fully elucidated.
The first known cell receptor for acetic acid is the free fatty acid receptor-2 (FFAR2), which selectively binds acetate and butyrate, but not proprionate. By comparison, the other SCFA receptor FFAR3 selectively binds butyrate and proprionate, but not acetate. Cross-signally mechanisms remain to be explored.
FFAR2 is a plasma membrane (the boundary/shell of a cell) transmembrane (crossing the membrane) protein (made up of amino acids and encoded by DNA) receptor (that binds signal molecule and signals into the cell) that is a member of the GPCR family. The GPCR family are G-protein coupled receptors, whose common features include a 7-times transecting of the plasma membrane, and a dependence on an intracellular G-protein for signal transduction.
The major signalling components known to be downstream of acetate signalling through FFAR2 include AMPK, cAMP, and adenosine-x-phosphate ratios.
