Genetic degradation - Carnivores lack taste for sweets

Carnivores lack taste receptors for sweets - An example of mutation driven devolution

https://www.nih.gov/news-events/nih-research-matters/carnivores-lack-taste-sweets

Excerpt: "Earlier research by Dr. Gary Beauchamp of the Monell Chemical Senses Center in Philadelphia showed that domestic and wild cats showed no preference for sweet-tasting foods. More recently, he and his colleagues reported that these cats have defects in the Tas1r2 gene, which codes for a key portion of the sweet taste receptor. The scientists reasoned that this malfunctioning gene might underlie the cats' reliance on a meat-based diet and indifference to sweeter plant-based foods.

To test this theory on other meat-eating animals, the researchers sequenced Tas1r2 genes from 12 species of non-feline carnivores (order Carnivora). The study was supported by NIH's National Institute on Deafness and Other Communication Disorders (NIDCD).
 

This was not the original design.

As reported in the March 12, 2012, online edition of the Proceedings of the National Academy of Sciences, 7 of the 12 tested species had flaws in the Tas1r2 gene. They include the sea lion, fur seal, harbor seal, Asian otter, spotted hyena and 2 cat-like creatures (fossa and banded linsang). All are strict meat eaters. These species, however, have differing mutations that disrupt Tas1r2. The researchers suspect that the gene may have been damaged and lost independently as these carnivores evolved toward exclusive meat-eating diets.

The remaining 5 species—including both omnivores and exclusive meat eaters—all had intact and functional Tas1r2 genes. These species include the spectacled bear, Canadian otter, raccoon, red wolf and aardwolf.

In behavioral tests, the researchers found that the Asian otter, with defective Tas1r2, showed no preference for sweet foods. But the omnivorous spectacled bear, with intact Tas1r2, strongly preferred foods with natural sugar or even no-calorie sweeteners."

A few examples of genetic degradation. Vertebrates lacking the sweet taste receptor:

SPECIES	DAMAGED GENE	TASTE	REFERENCES
African lion (Panthera leo krugeri)	Tas1r2	Sweet	Li et al., 2009
Cheetah (Acinonyx jubatus)	Tas1r2	Sweet	Li et al., 2005
Domestic cat (Felis catus)	Tas1r2	Sweet	Li et al., 2005
Asian small-clawed otter (Aonyx cinerea)	Tas1r2	Sweet	Jiang et al., 2012
Bats (31 species)	Tas1r2	Sweet	Zhao et al., 2010b, 2011
Spotted hyena (Crocuta crocuta)	Tas1r2	Sweet	Shi and Zhang, 2005
Tiger (Panthera tigris)	Tas1r2	Sweet	Li et al., 2005
Penguins (three species)	Tas1r2, Tas1r3,   Tas2rs	Sweet, umami,   bitter	Zhao et al., 2015
Vampire bats (genus Desmodus)	Tas1r2, Tas1r3	Sweet, umami	Zhao et   al., 2010b, 2011

https://www.sciencedaily.com/releases/2012/03/120312152639.htm

Excerpt: "The current research raises questions beyond diet choice, as taste receptors have recently been identified in many organs throughout the body, including intestine, pancreas, nose, and lungs. These extra-oral taste receptors are believed to serve many different functions."

My comment: Loss of information, damaged genes, loss of receptors, malfunctioning DNA strands, mutations etc. never result in any kind of evolution. These examples are hard evidence for genetic entropy. They also tell us that earlier in the history, thousands of years ago, these animals were able to eat plant based food. But because genetic degradation is an inevitable phenomenon all over nature, they have lost that ability and turned into carnivores.

Every example of a fossilized wing is FULLY developed and functional

Fossil record doesn't provide critical evidence for the theory of evolution

Evolutionary believers rely on fossil material as their final lifeline because they lack
scientific = observed evidence for their evolutionary tales. Arbitrarily combining fossils, constructing various imaginary lines of development, and sawing, drilling, or filing some fossils as needed, a credible line of development is achieved. This is how pseudoscience works.

Jurassic butterfly looks just like a modern butterfly.

However, there are problems that evolutionists are reluctant to raise in relation to fossil record. Some critical evidence is missing in the fossil record:

- Evidence for evolving insect wings

- Evidence for evolving butterflies or metamorphosis

- Evidence for evolving bird wings

- Evidence for evolving bacteria

- Evidence for evolving bat wings

- Evidence for evolving wings of flying fish

- Evidence for evolving flowers 

The fossil record doesn't show any evidence for assumed evolution. Instead, EVERY EXAMPLE OF A FOSSILIZED WING IS FULLY DEVELOPED AND FUNCTIONAL. A lack of transitional fossils was a big problem for Charles Darwin:

"Why, if species have descended from other species by fine gradations, do we not everywhere see innumerable transitional forms?"

The theory of evolution is the most serious heresy of our time. 

Variation without changes in DNA

Epigenetic regulation of alternative splicing

https://science-explained.com/theory/one-gene-many-proteins-alternative-splicing/

Excerpt: "Just as it is possible to make different dishes by using some ingredients but leaving out others, it is also possible to make different proteins by including or leaving out certain “ingredients” of genes. This process is called alternative splicing and it makes it possible to produce different proteins from the same gene (these different protein versions from the same gene are called isoforms). In this way, our bodies can produce over 100.000 proteins from only 20.000 genes." (My add: Probably millions of different proteins according to latest research.)

"But what about alternative splicing? The principle is the same, a pre-mRNA is produced and spliced, a 5’ cap is added and a poly-A tail is added. The only difference is, that instead of just splicing the introns out, some exons might be spliced out too. This leads to different proteins, one in which all 3 exons are used and one in which only exon 1 and 3 are used. So one gene for two proteins (see figure below).

The example discussed here concerns a gene with only 3 exons. Although this keeps the explanation simple, it does not provide the potential of many different isoforms. If we would have more exons that would mean more flexibility in the number of proteins that can be formed from a single gene. The gene Dscam from the fruitfly (Drosophila melanogaster) has 95 exons and can form 38.016 different proteins. So this one fly gene can form more different proteins than the number of genes we humans have in total!  

All in all, alternative splicing is an essential part of complex animals like us. The use of alternative splicing makes it possible to have many different proteins to fulfil all the different tasks necessary in our lives without the need of a gigantic genome."

Alternative splicing (AS) is regulated by epigenetic mechanisms:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6325479/

"Generally, AS can be coupled with transcription and subjected to epigenetic regulation, such as DNA methylation and histone modifications. In addition, ncRNAs, especially long noncoding RNAs (lncRNAs), can be generated from AS and function as splicing factors (“interactors” or “hijackers”) in AS."

My comment: Differences in the DNA are not the reason for human phenotypic variation. Genetically identical twins might have different colours of skin, hair and eyes. The most significant reason for variation in organismal characteristics can be found in epigenetic mechanisms and factors that regulate and mediate the alternative splicing mechanism. We should remember that genetically (DNA) all people are 99.9 % similar. The 0.1% difference is strongly related to hereditary diseases. This is why evolution believers hardly find fully beneficial DNA mutations. Evolution has no mechanism. Don't get lost.

Evolution believers confuse variation with evolution

It's a classical mistake to conflate change and evolution

Change in organisms is an observed fact and there's no reason to deny something very observable occurring in nature and in human beings, too. A good question is -- WHY change is happening and WHAT it results in. On these questions I'm focusing in this article.

Let's have an example familiar to everyone -- Dog breeding. We know that it's possible to have different dog breeds by so called artifical selection. This means silencing or amplification of certain, desired traits of dogs. Variation potential within canines is huge; during the last 200 years there have been more than 350 different dog breeds as a result of canine breeding. Also differences between traits and characteristics within breeds might be significant as this picture shows us. Both of them, the mighty Danish dog and the tiny Chihuahua have both descended from the Wolf.

But what has happened to canine genome? It's in a catastrophical condition within most breeds, especially those with a long breeding history. It means the more intense the breeding process the more genetic errors can be found in the genome. In other words, the more variation within stronger silencing/amplification of desired traits, the more genetic degradation.Within plants, the variation potential is huge. This is due to polyploidy and efficient epigenetic silencing of temporarily unnecessary DNA strands. A great example is Brassica oleracea. Over hundeds of years farmers have been breeding one plant into dozens of different varieties. These six common vegetables; brussels sprouts, broccoli, cabbage, cauliflower, kale and kohlrabi are actually the same plant -- the wild mustard plant. 

Epigenetic variation has nothing to do with assumed evolution. Change in organisms is based on epigenetic regulation of pre-existing biological information that often leads to minor genetic errors. In most organisms, loss and corruption of information results in reorganization of genetic information (genetic recombinations). This phenomenon accelerates speciation processes but also deepens genetic degradation making genomes weaker by genetic mutations. This is very observable also in human genome; there are 628,685 disease-related genetic errors but the number of beneficial mutations is close to zero.

Evolution has no mechanism. There is no scientific evidence for the man-made idea that increase in biological information pool could result in growth of structural or functional complexity in organisms. Variation, ecological adaptation, breeding etc. never create anything new. Traits and characteristics can be reshuffled but that's just reorganization of biological information based on environmental stimuli that affects cellular mechanisms such as receptors, signaling molecules and biological databases. Long-term scientific experiments have proved this fact. Don't get lost, my friends.

You can boost your immune system to fight the coronavirus

How to lower your risk of COVID-19?

https://theconversation.com/5-ways-nutrition-could-help-your-immune-system-fight-off-the-coronavirus-133356

"The coronavirus presents many uncertainties, and none of us can completely eliminate our risk of getting COVID-19. But one thing we can do is eat as healthily as possible.

If we do catch COVID-19, our immune system is responsible for fighting it. Research shows improving nutrition helps support optimal immune function.

Micronutrients essential to fight infection include vitamins A, B, C, D, and E, and the minerals iron, selenium, and zinc.

Vitamin D

https://www.researchsquare.com/article/rs-21211/v1

Excerpt from abstract: "Results: The mean level of vitamin D (average 56mmol/L, STDEV 10.61) in each country was strongly associated with the number of cases/1M (mean 295.95, STDEV 298.73 p=0.004, respectively with the mortality/1M (mean 5.96, STDEV 15.13, p < 0.00001).

Discussion: Vitamin D levels are severely low in the aging population especially in Spain, Italy and Switzerland. This is also the most vulnerable group of population for COVID-19.
 

Conclusions: We believe, that we can advise Vitamin D supplementation to protect against SARS-CoV2 infection.

https://www.cnet.com/how-to/the-surprising-role-vitamin-d-plays-in-your-immune-health/

Excerpt: "One of the main functions of vitamin D is to help activate T cells, aka the "killer cells" in the body. T cells actually detect and destroy foreign pathogens -- like viruses. "That makes vitamin D especially crucial for maintaining a functioning immune system that's capable of fighting back foreign pathogens," Tolentino says."

Vitamin A

Vitamin A maintains the structure of the cells in the skin, respiratory tract and gut. This forms a barrier and is your body’s first line of defence. If fighting infection was like a football game, vitamin A would be your forward line. 

We also need vitamin A to help make antibodies which neutralise the pathogens that cause infection. This is like assigning more of your team to target an opposition player who has the ball, to prevent them scoring.

Vitamin A is found in oily fish, egg yolks, cheese, tofu, nuts, seeds, whole grains and legumes.

Further, vegetables contain beta-carotene, which your body can convert into vitamin A. Beta-carotene is found in leafy green vegetables and yellow and orange vegetables like pumpkin and carrots."

B vitamins

https://theconversation.com/5-ways-nutrition-could-help-your-immune-system-fight-off-the-coronavirus-133356

"B vitamins, particularly B6, B9 and B12, contribute to your body’s first response once it has recognised a pathogen.

They do this by influencing the production and activity of “natural killer” cells. Natural killer cells work by causing infected cells to “implode”, a process called apoptosis."

Vitamins C and E

https://theconversation.com/5-ways-nutrition-could-help-your-immune-system-fight-off-the-coronavirus-133356

"When your body is fighting an infection, it experiences what’s called oxidative stress. Oxidative stress leads to the production of free radicals which can pierce cell walls, causing the contents to leak into tissues and exacerbating inflammation.
 

Vitamin C and vitamin E help protect cells from oxidative stress.

Vitamin C also helps clean up this cellular mess by producing specialised cells to mount an immune response, including neutrophils, lymphocytes and phagocytes.

So the role of vitamin C here is a bit like cleaning up the football ground after the game.

Good sources of vitamin C include oranges, lemons, limes, berries, kiwifruit, broccoli, tomatoes and capsicum.

Vitamin E is found in nuts, green leafy vegetables and vegetables oils."

Iron, zinc, selenium, green tea, black tea

https://theconversation.com/5-ways-nutrition-could-help-your-immune-system-fight-off-the-coronavirus-133356

"We need iron, zinc and selenium for immune cell growth, among other functions.

Iron helps kill pathogens by increasing the number of free radicals that can destroy them. It also regulates enzyme reactions essential for immune cells to recognise and target pathogens.

Zinc helps maintain the integrity of the skin and mucous membranes. Zinc and selenium also act as an antioxidant, helping mop up some of the damage caused by oxidative stress.

Iron is found in meat, chicken and fish. Vegetarian sources include legumes, whole grains and iron-fortified breakfast cereals.

Zinc is found in oysters and other seafood, meat, chicken, dried beans and nuts.

Nuts (especially Brazil nuts), meat, cereals and mushrooms are good food sources of selenium."

METHYL

https://www.whatisepigenetics.com/bolstering-your-defenses-against-covid-19-an-epigenetic-diet/

"Epigenetic Modulation of Host Response: Like other ssRNA viruses, when SARS-Cov-2 infects host cells, the virus requires continuous cellular transcription for viral mRNA synthesis. This mechanism implies functional association with the host’s genome expression so that it adapts the infected cell for the host-to-pathogen confrontation at each replication.[6] A key role is that RNA viruses can recruit host DNA methytransferases (DNMTs) to methylate and decrease gene function of specific genes including those for shaping innate and adaptive immune responses."

So, please take care of proper methylation.

The best examples of Intelligent design and Creation

Molecular motors, gears and other mechanical structures in living cells

1. Dyneins and kinesins, walking motor proteins, cargo-carriers (even 220 steps per second)
   
   https://www.sciencedirect.com/science/article/pii/S0006349508704685
   
   "Kinesin-1 and cytoplasmic dynein are the major cytoplasmic motors responsible for long-range transport in many cell types. Kinesin walks along microtubules toward the plus ends, facilitating material transport from the cell interior toward the cortex. Dynein transports material toward the microtubule minus ends, moving from the cell periphery to the cell interior."
    
   
   
   http://book.bionumbers.org/how-fast-do-molecular-motors-move-on-cytoskeletal-filaments/
   
    
   
    "This directed motion is made up of individual steps of 8 nm length, thus requiring about 100 steps per second to achieve such speeds in vitro."
   
2. MO-1 marine bacterium, seven ion-flow motors synchronized with a 24-gear planetary gearbox
   
   http://blog.godreports.com/2014/02/earliest-single-cell-bacteria-contained-seven-complex-motors/
   
   “The seven flagella propellers are inter-linked for minimum drag profile and maximum thrust by using 24 gears and a sheath, similar to modern aircraft and mufti-engine helicopters!” 
   
   
   “It actually has gears and it keeps all seven motors synchronized,” he notes. “Typically, any geared engines have no more than two motors. The best we could do in a helicopter is three engines and a multiple gear box to sync the engines.”
   
   “The motors can drive the MO-1 bacteria at relative speeds of 100 body lengths/second. A Cheetah achieves a land speed of only 25 body lengths/second in comparison and that’s in air, not fluid!” he says.
   
   
   
   
   
   
   
3. No known artificial machine can reach the energy conversion efficiency and sensitivity of this bio system
   https://phys.org/news/2006-02-bacterial-motors-nanotechnology.html
   
   "This motor has the same power-to-weight ratio as an internal combustion engine, spins at up to 100,000 rpm and achieves near-perfect efficiency. Yet at only 50 nanometres across, one hundred million would fit onto a full-stop. The only other natural rotary electric motor is in the enzyme ATP-synthase."
   
   https://www.advancedsciencenews.com/pinnacle-evolutionary-bionanotechnology-bacterial-flagellar-motor/
   
   "Experimental studies indicate that the energy conversion efficiency of the bacterial flagellar motor is very high. Nearly the complete energy released by the protonmotive force is converted into mechanical rotation." 
   
   
   "A signaling molecule becomes phosphorylated and the change of the phosphorylated cytoplasmic concentration then causes the rotation to switch between CCW to CW. The bacterial flagellar motor is remarkably sensitive and already small changes of the phosphorylated protein concentration result in conformational changes and so in a change of the direction of the rotation within milliseconds."
   
   
   

My comment: The energy conversion efficiency of rotary molecular motors is much higher than that of man-made motors. How could blind, random forces be able to produce such energy conversion solutions? How could random chance be able to construct a proton pump? These super complex electromechanical machines point to Intelligent Design and Creation. And what makes them far too complex for human engineers is that they are able to reproduce. Don't get lost my friends.

The first empirical evidence of the importance of epigenetic variation during the emergence of new species

Epigenetic mechanisms and factors behind speciation - No evolution observed

A fresh study confirms that epigenetic mechanisms and factors might result in rapid speciation within Cichlid fish:

https://cordis.europa.eu/project/id/659791/de

Excerpt: "Phenotypic plasticity plays a key role at the onset of the speciation process, facilitating diversification though the induction of novel phenotypes in response to distinct environments. Via genetic accommodation and genetic assimilation, this influence may extend throughout the speciation process and beyond, into subsequent speciation events. While the epigenetic regulation of gene expression that mediates phenotypic plasticity has been extensively studied in lab-based model organisms, very little is known about epigenetic variation in natural populations. This project will be the first epigenetic study explicitly focused on the speciation process. Using cutting-edge techniques, the applicant will characterize DNA methylation variation within and among the sympatric species of a recently discovered endemic cichlid fish radiation in Lake Massoko, Tanzania. Specifically the applicant will test: if

1) newly formed species differ in the distributions of epigenetic marks across the genome,

2) genomic variants linked to phenotypic divergence among species are in genomic regions unusually high in DNA methylation, as expected under a hypothesis of epigenetic differences preceding fixed nucleotide differences during adaptive divergence,

3) genomic regions diverging in patterns of methylation among incipient species are also exhibiting high levels of methylation in populations of Astatotilapia calliptera, the ancestral, colonizing species. 

 

The results of this pioneering project will provide the first empirical evidence of the importance of epigenetic variation during the emergence of new species."

My comment: Epigenetic modifications never result in any kind of evolution, because

1. Adaptation is based on epigenetic regulation of pre-existing biological information that often results in

2. Subtle errors in passive DNA, which often leads to

3. Reorganization of biological information (genetic recombinations, epigenetic recombinations)

Epigenetic adaptation can sometimes be observed as changes in phenotype. This is not evolution because organisms experience variation within their own kinds (Taxonomic rank: A family, sometimes a genus). There is NO scientific (observed, verified, measured, repeated) evidence for the evolutionary idea that increase in biological information could result in growth of structural or functional complexity in an organism. That's why speciation is not evolution. Several empirical experiments (Lenski, Drosophila etc.) prove this biological fact. Don't get misled, my dear friends.