PFTS Syndrome
Peri-weaning failure-to-thrive syndrome (PFTS) is a poor growth syndrome in piglets around birth. It occurs intermittently or continuously in virtually all pig farms. It affects 5 - 15 % of the herd. Symptoms include lethargy, anorexia, feed refusal and death by starvation due to faeces without an infectious cause. Numerous studies in different countries have ruled out all potentially harmful infectious diseases. Specific pathogen-free (SPF) herds with a high animal health status are similarly susceptible to disease as the average livestock herd. Piglets born by caesarean section in a gnotobiotic model and reared without colostrum also show PFTS syndrome. A typical symptom is polyserositis (simultaneous inflammation of several acid membranes and developmental anomalies of rapidly proliferating mucosal epithelial, glandular and brain cells). It is also known as Concato's disease. The catabolic processes are disrupted so that the body's reserves are exhausted.
Typical lesions:
- Inflammation of the gastric mucosa and atrophy of the intestinal mucosa (villous atrophy)
- Atrophy of the serous cells that secrete yellow-forming mucins in the colon mucosa
- Inflammation of the nasal mucosa
- Thymus atrophy (atrophy of the thymus)
- Meningitis of unknown cause (non-suppurative meningoencephalitis)
If the mitochondria do not function properly, the cells lack energy and tissues and organs cannot function properly.
There is a connection between Arginine deficiency and thymus atrophy. In the case of thymus atrophy, too few T lymphocytes are produced. As a result, the piglets die or have to be euthanised in accordance with animal welfare regulations due to their severe debilitation. (Yanyun Huang, Henry Gauvreau, John Harding 2011; 2012).
The symptom complex is known in human medicine as mitochondrial disease and is very similar to PFTS syndrome.
Niacin is found in every cell of the body
Nicotinic acid or Nicotinamide is an active compound that builds up dehydrating and oxidising enzymes. Another active form is the reversible hydrogen carrier nicotinamide adenine dinucleotide (NAD+). These enzymes play a crucial role in intermediary metabolism, which is essential for the function of the enzymes involved in cellular respiration.
Without nicotinamide, the breakdown and synthesis of fatty acids, carbohydrates and Amino acids not correct.
As most of the Intestinal bacteria In order to be able to synthesise nicotinic acid from the amino acid tryptophan, the intestine must be in good condition. If the intestine is in a state of dysbiosis (lack of beneficial intestinal flora), it cannot synthesise niacin (nicotinic acid) from tryptophan. In this case, the intestinal mucosa is damaged. Not enough tryptophan and nicotinic acid are absorbed (60 mg tryptophan = 1 mg nicotinic acid).
Tryptophan and nicotinic acid are precursors of nicotinamide
They are used in the Liver are converted into active nicotinamide and play a role in the synthesis of sex hormones. The body needs nicotinamide for the synthesis of Oestrogenprogesterone and testosterone.
Dr Judit Mária Molnár is a professor at Semmelweis University of Medicine in Hungary, where she studies mitochondrial diseases. These can occur as early as childhood and can be very severe. The disease is usually milder in adulthood. Symptoms include drooping eyelids, muscle weakness, muscle atrophy, epilepsy, various endocrine disorders, anaemia of unknown cause, coordination disorders and psychiatric symptoms.
The dysfunction of cellular mitochondria is partly hereditary, but acquired mitochondrial defects caused by environmental and nutritional factors are also becoming increasingly common. According to researcher Douglas Wallace, the accumulation of mitochondrial damage leads to diseases of civilisation and ageing (Wallace, 2005).
Most illnesses occur between the ages of 40 and 50 and physical decline begins between the ages of 50 and 60.
The daily human requirement for tryptophan is 250-500 mg. 94% of this essential amino acid is used in the production of NAD+.
Environmental changes influence the availability of the amino acid tryptophan
The most commonly used herbicide worldwide is Glyphosate. It inhibits the production of tryptophan and phenylalanine (essential aromatic amino acids). These are formed via the shikimate pathway in plants, bacteria and some fungi.

Intestinal bacteria also metabolise the essential amino acid tryptophan and thus improve the availability of tryptophan for the host. The effect of glyphosate prevents this. (O'Mahony et al; 2015); (Martin et al; 2018); (Anthony Samsel and Stephanie Seneff 2013).
About glyphosate and its adverse effects
GMO food plants and animal products from animals that have been fed with GMO feed plantscontain glyphosate. Glyphosate kills beneficial intestinal bacteria (Enterococcus, Bacillus, Bifidobacterium, Lactobacillus) and inhibits the growth of tryptophan-producing intestinal bacteria. Clostridia, E. coli and salmonella multiply excessively when they come into contact with glyphosate.

Enterotoxins cause inflammation of the intestine. Neurotoxins damage the peripheral nervous system (PNS) and the central nervous system (CNS) and alter the permeability of the blood-brain barrier (BBB).
As a result of the physiological problems caused by 70 years of chemical farming and almost 30 years of GMO agriculture The lack of nicotinamide in farm animals is caused by feed materials and additives from the feed industry.
Today's eating habits, chemical and genetically modified food production as well as unnatural feed and food additives (e.g. free amino acids) cause physiological problems. These have led to a malfunction of the Kynurenine metabolisms led.
For example, the amino acid lysine, which is used as a free amino acid, leads to a higher lysine content due to the lysine-Arginine-antagonism leads to a local arginine deficiency. The NO deficiency hinders the first step of the kynurenine pathway (conversion of tryptophan into kynurenine). Indoleamine 2,3-dioxygenase (IDO) catalyses this process. (Hao Wu Jianping and Gong Yong Liu, 2018).

