The effect of Wendelin essencia hepar on the birth weight of piglets and the vitality of piglets:
I try to answer the questions based on the data evaluation of tens of thousands of litters by dozens of researcher and analyst experts in several countries.
How can we avoid low birth weight piglets?
The formulation of a long term strategy is necessary, we can achieve this by the reevaluation of the replacement gilt selection method.
There is also a method providing short term result, which prevents the regeneration of the problem, this eliminates insufficient placenta function that appears as a consequence of pig nutrition physiological flaws. We can achieve the birth of piglets with optimal birth weight, vitality and immune condition by giving the pregnant sow wendelin essencia hepar to drink.
The individual piglet with birth weight of over 1.4-1.5 kg has a good chance of survival, a good rearing indicator, and when female individuals serve they have a good reproductive performance and phenotypically do not preserve the occurrence of low birth weight piglets.
At the Congress of the International Pig Veterinary Society (IPVS) in Dublin, in June 2016, Jourquin presented research results from Spain. 2,331 litters were examined till weaning, the data of 178 litters were monitored from birth to slaughter.
The average total born piglets per litter was 14.3, of which 13.1 were live-born. The average birth weight was 1.46 kg. Prewean mortality was 17.5%. According to their study they found 1.13 kg to be the critical piglet birth weight, where there is a clear break point. In the case of piglets under this weight prewean mortality considerably deteriorates. For piglets under the 1.13 kg/individual weight the chance of survival was 58%; in the case of individuals over this weight the chance of survival was 92%.
Miranda Smit, a researcher at the University of Alberta, gave a lecture in 2012 about the role of optimal litter size in weaning and fattening results. The birth weight of a piglet has a defining role in the subsequent development of the individual. She classified piglets into 3 categories according to birth weight. She classified piglets into the low birth weight (LBW), medium birth weight (MBW) and high birth weight (HBW) categories. The average birth weight of the piglets was 1.2 kg/individual, 1.4 kg/ individual, 1.8 kg/individual respectively.
Between the low and high birth weight individuals there was a 0.81 kg/individual weight difference at weaning 21 days after birth, after leaving nursery 65 days after birth the difference was 3.05 kg/individual, at the weight measurement 149 days after birth it was 6.92 kg/individual. The performance difference was especially significant between medium and low birth weight piglets.
There was also a considerable, nearly 10 day, difference in reaching the slaughter weight (115.8-116.2 kg). She also found a significant difference in prewean mortality: in the high birth weight HBW group mortality was 6.7 %, in the low birth weight group mortality was 16.4 %.
According to research results published by Emma Baxter et.al (2010), low birth weight is the greatest risk related to prewean piglet mortality. According to the author this affects nearly 2 million piglets in the United Kingdom. In the case of optimal birth weight piglets, 1.5-2.1 kg/individual, the chance of survival till weaning was 85-89 %, the chance of survival till weaning of piglets with 1.0-1.5 kg/individual weight was 53-88 %. The chance of survival till weaning of piglets with 0.5-1.0 kg/individual weight was on the average only 25 %.
Horst Brandt published similar research results. Based on results from Germany, in the suckling and weaning period, piglets with individual weight below 0.8 kg had a mortality of 55 %, while piglets with individual weight below 1.0 kg had a mortality of almost 30 %. Sandra Edwards & Emma Baxter cite the results of Roehe and Kalm (2000), Scottish Agricultural College, Edinburgh, members of the Sustainable Livestock Breeding Research Group. They studied the correlation between birth weight and survival for two generations. They evaluated the results of the 1st–3rd farrowing of proportional age distribution sows. The first litter sizes were between 12.8 and 13.1. They analyzed the data of 21, 835 live-born piglets.
Piglets with a birth weight of 1.0 – 0.5 kg had 30-83 % mortality till weaning.
At the University of Alberta Pig Technology Research Center in Canada, J.Patterson researched the role of the birth weight of piglets in their later lives. He studied the effect of birth weight on the animal’s own life, and in the case of female individuals that served as sows, the effect on prolificacy performance. In his opinion low birth weight piglets suffer from „Intra-Uterine Growth Retardation”.
The anatomic cause of Growth Retardation is that the placental weight of low birth weight piglets is low, and the low birth weight is the consequence of low placental weight.
/ The pathological causes of piglets with IUGR are described later./
The next figure well illustrates that low birth weight has only an insignificant effect on the weight of the brain, while visceral organs lose a higher amount of their weight, in their proportion the weight decrease of the intestine, liver as well as muscle exceed the decreasing of birth weight.
According to the research of Alvarenga et al. (2012), the duodenal mucosa of piglets with low birth weight is considerably lower than those of piglets with high birth weight not only at birth but also at the age of 150 days. The development level of the duodenal mucosa makes the effectivity of digestion questionable in the case of low weight piglets.
Birth weight determines the period of the serving of the animals. The gilts reared from low birth weight piglets only get pregnant from the first parity and become breeding sows at the rate of 37 %, only c.a. 15 % of individuals taken into serving reach the 6th farrowing. In contrast with individuals with high birth weight, which get pregnant in the first parity period at the rate of 85-90 %. The sows that were piglets with high birth weight reach the 6th farrowing at the rate of 40 %.
According to the not published data by Linck Monori, the uterine weight of low birth weight piglets is c.a. one half of the uterine weight of high birth weight piglets.
In the National Pig Research Program of the US, in 2015 J. Pattersen and his colleagues studied what kind of correlations there are between high prolificacy, medium prolificacy and low prolificacy litters and the occurrence of extreme low birth weight piglets. The figure illustrates that in the case of litters with 10 total born piglets or more, in the litters the proportion of extreme low birth weight piglets is 20 %.
Based on the above description the correlation is not clear, piglets with extreme low birth weight are not just the result of the increase in the number of the total born piglets.
It is clear that with the increase of the number of total born piglets the birth weights of piglets decreased. Frequently we say, just to reassure ourselves, that the piglets are small but prolificacy is high, they will grow.
Unfortunately they don’t grow, 47 % of low birth weight piglets don’t reach slaughter weight, if they don’t die then they grow suffering from many problems, they reach slaughter weight late thus rearing deteriorates. The efficiency of breeding also deteriorates, since only 38 % of them serve.
In a herd a serious problem occurs when gilts reared from low birth weight piglets enter the breeding in high numbers.
Texas A&M University of Agriculture and the Chinese Beijing University of Agriculture have published joint research results about the homogeneity of piglet birth weights within a litter.
They were searching for and found a correlation between the nutrition conditions of the sow and the increase in the proportion of piglets with low birth weight.
They processed 158 professional literature articles to gain an understanding of the development of the problem, the description of physiological processes and the correlation with sow nutrition. According to their conclusion a very strict correlation exists regarding the fact that under a critical piglet birth weight the survival of piglets till weaning is minimal.
(I list the accessibility of the article among professional literature sources, I also publish the references of the article, so everyone can study it.)
They introduce a concept citing the processing of 10 professional literature articles: Intra Uterine Growth Retardation (IUGR). In their opinion the reason for low birth weight piglets is growth retardation that occurs as a result of some kind of pathological causation. The drawings show the skull profile of a piglet suffering from IUGR. Inside the uterine the growth of the brain enjoys priority, thus the brain skull of the piglet with growth retardation fully develops but the face skull connected to it is not developed to the sufficient size. On the photo an IUGR affected piglet born with concave nose top.
We should pay attention to this phenomenon, because it is of indicative value showing that there is a problem in the development within the uterine.
After the formation of the placenta’s blood vessels the increase in the density of blood vessels is especially significant between 90 and 110 days of pregnancy. Insufficient blood vessel density of the placenta has a harmful effect on the development of the fetus, it hampers the reaching of optimal birth weight (Argente et al., 2008). As a result of insufficiently functioning vasodilatation, the weak blood supply of the placenta limits the development of the piglets (Argente et al., 2006; Foxcroft et al., 2007).
Both factors, angiogenesis, the development of the blood vessels, and the vasodilatation of the blood vessels are of key importance in the blood supply to the piglets. What are the physiological factors that affect extreme low birth weight and low weight piglets?
Batshaw and Brusilow published as early as in 1978 that the high ammonia level (hyperammonemia) of umbilical blood results in low birth weight in piglets as well as in human babies, and it may even endanger the survival of the fetus inside the uterine.
In the case of fetuses suffering from IUGR, fetuses with growth retardation, between the 90th and 110th day of the pregnancy the ammonia level of the umbilical vein was significantly higher than in the case of normal birth weight piglets (Lin et al., 2012).
Here I would like to interject.
Nowadays even in Hungary and in the world it is a general phenomenon that the mouths of sows are foaming (frothy saliva) and they have a chewing mouth movement.
This phenomenon is ammonia toxicity, you can study this in detail on the Wendelin-essencia homepage:
Sows foaming at the mouth (frothy saliva), photos from Canada, Europe, Australia
Sows foaming at the mouth (frothy saliva), I made photos from Europe and Hungary
Sows foaming at the mouth (frothy saliva), I made video from Europe and Hungary
Sows foaming at the mouth (frothy saliva), video from Canada
What causes ammonia toxicity?
1. If there is an insufficient amount of healthy liver cells then ammonia decomposition is inefficient in the liver, urea synthesis is on an insufficient level in the urea-cycle, thereby ammonia accumulates in the blood. Thus nowadays liver protection is very important in the case of pregnant sows.
2. In the urea-cycle the ornithine → arginine, ornithine absorbs ammonia from the blood in a multiphase transformation, then by the activity of the arginase enzyme it produces the non-toxic urea that can be excreted by the kidneys while arginine transforms back into ornithine. The antagonism of lysine-arginine and the lysine-arginase enzyme create a disruption in this process.
So, the foaming of the mouths of the sows is not a behavioral anomaly, rather the result of obstructed ammonia-urea transformation appearing because of arginine shortage caused by the liver condition of the sows (hepatic encephalopathy), and lysine-arginine antagonism.
If the mouth of a sow is foaming then the uterine placenta’s angiogenesis and vasodilatation are impaired because of the following physiological correlation, if the urea-cycle is not functioning then Nitric Oxide synthesis is not functioning either:
The cause of the insufficient birth weight and low vitality of piglets, the weak immune condition of young piglets and their problematic rearing, is the high ammonia level of the blood, as well as placenta angiogenesis and vasodilatation impairment caused by arginine shortage.
The development and growth of the fetus is a complex biological process that is influenced by genetics, the physiological condition of the mother, the sow’s rearing circumstances, its nutrition during pregnancy and other environmental impacts (Redmer et al. 2004). These factors influence the embedding of the zygote, the formation of the placenta, the development of the placenta’s blood vessel network, angiogenesis. Within the uterine the functioning of the placenta, the vasodilatation of blood vessels, the efficiency of nutrient transport and gas replacement have a defining effect on the development of piglets (Bell and Ehrhardt,2002; Fowden et al.,2005 ; Reynolds et al.,2006; Wu et al. 2006).
Fetal and maternal circulation in the placenta:
Wu, G. research project leader at Texas A&M University, Animal Science Institute, published the following article in 2008:
Low birth weight (LBW) piglets weigh less than 1.1 kg, their occurrence proportion in the US is 15-25% of newborn piglets. In the case of these piglets the growth and development of the luminal mucosa is impaired. In the case of these piglets growth and development deteriorate, body growth decreases, the rate of still births and death between the 1st - 3rd day after farrowing increases. Despite the fact that this is a significant problem in pig production, currently no effective method is available to improve the survival rate of LBW piglets, because the involved mechanisms are mostly unknown. We assume that arginine promotes intestinal growth, thus the development of sufficient weight piglets. Arginine reduces the ammonia level of fetal blood (ammonia is extraordinarily toxic for the developing fetus), thereby it increases the survival rate and growth of low weight LBW piglets.
A change occurring in arginine metabolism has a positive effect on the above described problems. The result will expectedly have a significant impact on US pork production, because this improvement enables producers to obtain such practical instruments that are useful in the management of the problems caused by low birth weight piglets.
They examined the impact of arginine addition on the birth weight, development level and vitality of piglets by creating optimal rearing and nutrition conditions. The physiological reason for arginine addition is the fact that arginine serves as the exclusive donor in nitrogen monoxide synthesis which is the neurotransmitter of vasodilatation and angiogenesis. L-arginine is an important precursor to nitrogen monoxide synthesis (Wu and Morris, 1998; Wu and colleagues., 2007; Blachier et al., 2011). Both play a key role in the growth of the placenta and in its angiogenesis (Wu et al., 2006). Thereby blood flow improves 11 and the placenta functions more efficiently, the nutrient supply to the fetuses improves, especially in the case of the piglets positioned far from the uterine tube. The homogeneity of the litter improves, the weight of the piglets becomes more homogeneous, the occurrence of extreme low birth weight piglets decreases (McCrabb and Harding, 1996; Gardner et al., 2001; Mateo et al. 2007; Gao et al., 2012; Wu et al. 2013).
There are numerous research results regarding the effect of arginine additives during pregnancy increasing the number of live-born piglets as well as the birth weight of piglets.
The effect of arginine additives in feed with high lysine free amino acid content on the total number of piglets born in the litter as well as litter weight was studied. 52 gilts were involved in the study.
The total number of live-born piglets increased by 22 %, litter weight was 24 % higher. The average stillborn piglets per litter of 1.86 dropped to 0.66/litter as a result of arginine treatment. The average weight of live-born piglets increased by 4 % (R.D.Mateo et al. 2007).
Gao, K., Jiang, Z., Lin, Y. and his research team published extraordinarily encouraging results in 2010. In their article they studied the fetal survival and growth problem in 108 pregnant sows. According to their hypothesis the addition of arginine between the days 22 – 114 of the pregnancy would improve the placenta’s growth, functioning and nutrient supply. By comparison with the control group, arginine significantly (P <0.05) increased the total number of born piglets by 1.31 piglets, the number of live-born piglets per litter increased by 1.10 piglets. The average weight of live-born piglets in the group that received arginine additive treatment was 1.70 kg. In the arginine treated group the weight of the placenta was significantly (P <0.05) higher, by 16.2%. These results show that the arginine given as an additive favorably improves the growth of the placenta and the reproductive performance of sows.
The problem of young age immune condition is connected to the low birth weight problem of piglets which is also related to arginine deficiency. Arginine additive improves immune condition, and it results in the most optimal immune-biological condition in the case of pregnant sows and newborn piglets, thereby reducing morbidity and mortality by exerting suitable immune response to infectious pathogens (Han et al. 2008 ; Li et al. 2007 ; Tan et al. 2008).
I describe countless pathophysiological processes connected with arginine deficiency on my homepages:
Here I would like to make a few statements in connection with this:
The problems that can be traced back to this metabolic pathophysiological condition are the following:
A solution option in Wendelin essencia hepar for problems affecting the circulatory organ system.
The weight problem of newborn piglets and the connected pathophysiological processes:
Wendelin essencia represents new and effective assistance in these syndromes.
Why isn’t a sufficient amount of Nitric Oxide produced?
Let’s take a look at the physiological foundation of this:
Why isn’t there a sufficient amount of arginine in the sow’s body?
In this lysine dominant condition how is it possible to deliver arginine into the body?
In relation to the digestion and diffusion of proteins animal feed professional literature frequently contradicts physiology, specifically in the digestion and diffusion of proteins and amino acids. Amino acids within proteins are diffused more easily as peptides than as free amino acids. There is a significant reason for this, peptides are absorbed by simple diffusion, without energy requirement, by passive transport.
Free amino acids are diffused by means of membrane transporter proteins, the so-called carrier molecules, and Na+ pump. It’s the consequence of free amino acid diffusion by the mediation of membrane transporter proteins, and lysine-arginine antagonism, that the absorption of free amino acids isn’t unproblematic, and because of the lysine dominated pig feed the animals suffer from permanent arginine deficiency.
Fulvic acid is the lowest molecule weight fraction of humic acids, it has two favorable characteristics for us.
These two characteristics make it possible to avoid the lysine-arginine antagonism by giving the arginine to the animals in the form of arginine-fulvic acid complex. We utilize this physiological mechanism to deliver the arginine.
The essencia added to drinking water mixes with the feed in the stomach. The amount of fulvic acid in wendelin essencias also makes it possible for the free amino acids in the feed to be absorbed, especially as two base lysine, fulvic acid-lysine complex form. Thereby the finite membrane transporter proteins are also available for arginine.
The presence of arginine enables angiogenesis and the functioning of vasodilation.
Wendelin essencia has two different amino acid metabolism characteristics:
1. This protected arginine delivery is present exclusively in Wendelin essencia.
2. The mechanism whereby the lysine in the feed is absorbed not as a free amino acid, rather as fulvic acid-lysine complex, eliminates the problem of lysine-arginine antagonism.
Both conditions are important and indispensable.
This effect functioning on a physiological basis gives hope for the better development of placenta blood vessels of pregnant sows, their angiogenesis and the better dilation of blood vessels. As a consequence of this, based on research results the placenta weight increases by c.a. 25 %, the number of live-born piglets increases by 22 %, and the litter weight increases by 26 %. The number of extreme low birth weight nonviable piglets decreases.
The black cranberry leaf contained in wendelin essencia hepar contributes to the improvement of the vasodilation ability of blood vessels. In the cranberry the anthocyanins, pro-anthocyanins, leucoanthocyanins, flavonoids and their derivatives have bioactive characteristics, they stimulate collagen synthesis which contributes to the elasticity of blood vessels. Thereby the cranberry promotes the maintenance of the healthy vasodilation of blood vessels.
The liver protecting function of wendelin essencia hepar provided by Mary-thistle is indispensable for the reduction of blood ammonia level in sows, and the presence of the optimal quantity and healthy liver cells.
The next study discusses the physiological role played by NO as a neurotransmitter in the body:
" NO" The role and functions of living organisms
Marcin Magierowski, Katarzyna Magierowska, Slawomir Kwiecien and Tomasz Brzozowski Department of Physiology, Jagiellonian University Medical College, Cracow 31-531, Poland Received: 20 March 2015 / Accepted: 13 May 2015 / Published: 19 May 2015.
In the figure there are several correlations involving the physiological role played by NO as a neurotransmitter:
In the macrophages of the immune system (phagocytes) the Inducible Nitric Oxide Synthase enzyme synthetizes NO. It exerts its effect when the cell devours a pathogen. Its task is to destroy the pathogen. As a result of its large quantity NO production the iNOS has a cytotoxic effect. The NO produced in the macrophages has an antimicrobial and tumor cell damaging effect. The iNOS production of the macrophages is initiated by cytokines of the Th1 immune response, the LPS antigenic effect of bacteria, as well as antibacterial toxins. Nitrogen monoxide exerts its cytotoxic effect by preventing the proliferation of bacteria as well as virus replication, as it blocks the functioning of the key enzyme of DNA and RNA synthesis, ribonucleotide reductase.
Based on the physiological effect of wendelin essencia hepar, by providing essencia during pregnancy to breeding sows lysine-arginine antagonism can be reduced, thus NO deficiency doesn’t develop in the animals. In the breeding sows every 150-160 days the process of angiogenesis in the development of the placenta will be optimal, thus the birth weight of piglets will be characteristic of the pig species, this is particularly important in the case of proliferous genotype species and hybrids.
The physiological syndromes of pig nutrition by age groups:
Problems of the breeding sow:
Placenta blood vessel angiogenesis and vasodilation impairment:
Problems in weaned piglets:
Problems in fattening pigs:
1. Jourquin, Jan: Piglets born at a weight below 1.13 kg have been found to have a substantially decreased chance of survival. International Pig Veterinary Society (IPVS) Congress held in Dublin, Ireland, 7-10 June, 2016.
2. Horst Brandt . Individual piglet birth weight Institute for Animal Breeding and Genetics, University of Göttingen, Albrecht-Thaer-Weg 3, 1998. 37075 Göttingen, Germany
3. Emma Baxter et al. 2010 : Improving Piglet Survival, SAC Pig Research Workshop,
4. Roehe R and Kalm E 2000 Estimation of genetic and environmental risk factors associated with preweaning mortality in piglets using generalized linear mixed models. Animal Science 70: 227-240
5. Tao-lin Yuan,1 Yu-hua Zhu, Meng Shi,1 Tian-tian Li, Na Li, Guo-yao Wu, Fuller W. Bazer, Jian-jun Zang,1 Feng-lai Wang,1 and Jun-jun Wang: Within-litter variation in birth weight: impact of nutritional status in the sow, J Zhejiang Univ Sci B. 2015 Jun; 16(6): 417–435.
6. L. Che, P. Yang, Z. Fang, Y. Lin, D. Wu: Effects of dietary arginine supplementationon reproductive performance and immunity of sows, Czech J. Anim. Sci., 58, 2013 (4): 167–175
7. Miranda Smit PhD candidate, University of Alberta: optimal litter size-Incrasing the numberof quality pigs weaned, Saskatchewan Pork Industry Symposium 2012
8. Norton C, Kalea A, Harris P, et al. Wild blueberry-rich diets affect the contractile machinery of the vascular smooth muscle in the Sprague-Dawley rat. J Med Food. 2005, 8;(1):8-13
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