by Lucien Tuinstra

Many thanks again to Creation Ministries for another fascinating article showing with utmost clarity the impossibility of Darwinian “evolution”. When you subscribe to Creation Magazine you also receive daily e-mails, such as these, to strengthen your Biblical beliefs.

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Gibber! Gibber!

Chugley

The liver is a multifunction accessory organ to digestion, which means that it is not part of the alimentary canal, but external to it.¹ Among other things, it is essential to the healthy functioning of the gastrointestinal and endocrine systems. Introducing digestive juices into the system, liver functions are part of the process of detoxifying and breaking down food components into a form suitable for absorption. Examples of absorbed nutrients are amino acids, mineral salts, fat, and vitamins. These are building blocks for new cells, hormones, and enzymes, as well as an energy source for other processes.

A selection of functions

The liver has many roles important for the organism’s survival: “Liver functions are pivotal to homeostasis and involve interactions with most of the body’s organ systems.”¹ For brevity, a few of them are described here.

Carbohydrate metabolism

The liver controls the glucose level in blood by converting glucose into glycogen (glycogenesis) if the glucose level is too high, and vice versa when it is too low. When a person has low blood sugar, the liver can release glucose through the conversion of certain amino acids and lactate, as well as other sugars like fructose and galactose. If the sugar level is too high, the liver can turn glucose into fats, too.

Protein metabolism

The compound adenosine triphosphate (ATP) delivers energy for most of life’s metabolic processes; for example, the manufacture of protein machines. ATP synthase is one such machine, a motor consisting of 29 proteins, which in turn produces ATP.²

Besides accounting for almost a fifth of total body protein synthesis (including ATP synthase),³ the liver can digest proteins and convert the resultant amino acids into fat, which it is able to store for later use. The initial step in this breakdown process is the deamination of the amino acid, by removing the amino moiety (NH₂), with by-products co-opted into ATP production. At a pH of 7, and even more so in an acidic environment, the alkaline NH₂ is quickly protonated (H⁺) into the toxin ammonia (NH₃),⁴ which the liver converts to the much less toxic urea, disposed of in urine.

Removal of drugs and hormones

A very important function of the liver is the detoxification of drugs such as penicillin, sulfonamides (R–S(= O)2–NR2, with ‘R’ a chemical group, the simplest being hydrogen), and ethanol (alcohol). It can also chemically change thyroid and steroid hormones, such as estrogens and aldosterone.

Excretion of bile

The hepatic cells of the liver daily produce nearly 0.5 litre of bile;⁵ a basic liquid (pH 7.6–8.6) that has a yellow, brown, or olive-green colour. Bile is needed for fat digestion during and after meals, so is stored in concentrated form in the gallbladder. This secretes about 500 ml of bile per day, a rate that is regulated by the hormone cholecystokinin (CCK), which causes the gallbladder to contract. Bile is mainly water with bile acids and other salts, cholesterol, bile pigments, ions, as well as other materials. The bile salts help the cholesterol to dissolve in the small intestine. Through their emulsifying action on fats, they also break down large fat globules into smaller droplets, as well as preventing the latter coalescing into larger ones. This increases the lipid surface area for hydrolysis by the pancreatic enzyme lipase. Hepatic lipase controls fat levels in the blood. The bile pigment bilirubin derives from the breaking down of red blood cells (RBCs), as does iron (figure 1). In the intestine, bilirubin gets further broken down into urobilinogen, giving faeces their characteristic brown colour. In diseases where bilirubin removal from the liver is restricted, it collects in other body tissues, giving the skin and eyes a yellow colour (jaundice).

Storage

Not only is the liver a storage place for the aforementioned glycogen and fat, it also stores iron and copper, and it contains reservoirs of vitamins A, B12, D, E, and K. Together with the skin and kidneys, the liver activates vitamin D.

Production of heat

With all these activities, it is not surprising that the liver uses a significant amount of energy. With its high metabolic rate, the liver is the main heat-producing organ of the body.

Evolution of the liver

According to Johns Hopkins Medicine, “More than 500 vital functions have been identified with the liver.”⁶According to Johns Hopkins Medicine, “More than 500 vital functions have been identified with the liver.”

It beggars belief how all this could have come about in a gradual, goal-less, evolutionary progression. From no liver to a fully developed, integrated, multi-tasking organ, numerous tasks would need to be put in place, all interdependent with other organs/systems. This would require the successful implementation of a fantastic number of incremental mutational changes.

Unlike other human visceral organs, the liver can fully regenerate after partial tissue loss:

“Liver regeneration involves a complex network where diverse signaling pathways from different cell types regulate the precise control of genes encoding transcription factors needed to recover the hepatic mass.”⁷

If regeneration from a reduced liver is complex, how did this organ arise in the first place?

Phylogeny studies of vertebrate livers are scanty.⁸ A popular textbook for vertebrate comparative anatomy, commenting on the liver in a range of organisms, says that its shape “conforms to the space available in the coelom”.⁹ This is akin to saying a round peg fits in a round hole. It does nothing to explain either the arrival of the peg, or the hole.

Liver evolution putatively commenced in an ancestral organism probably similar to the lancelet Amphioxus, part of the Cephalochordata sub phylum and, according to evolutionary thinking, the closest thing to a vertebrate. “The recent discovery of vertebrate liver-specific proteins in the Amphioxus diverticulum supports this hypothesis.”¹⁰ What, then, might be ancestral to the diverticulum? The reason that “this question is traditionally omitted is that the putatively preceding forms (living animals or fossils) apparently do not provide any relevant evidence for the answer”.¹⁰

Pinnacle of liver evolution?

A “mutation of a key enzyme involved with the breaking down of glycogen into glucose in the liver … would spell death or a serious problem for the individual”.

The healthy human liver does a mighty job, and, by all accounts, it is at peak performance. But assuming evolution brought us to this point, why stop at this apparent summit? Do mutations cease when an organ is functioning well? Unfortunately, mutations are part of life in a cursed creation. A “mutation of a key enzyme involved with the breaking down of glycogen into glucose in the liver … would spell death or a serious problem for the individual”.¹¹ Mutations are more often than not deleterious,¹² and they have very rarely, if ever, been shown to add any significant genetic information.¹³

Examples of Mendelian liver diseases, caused by hereditary mutations, include haemochromatosis (too much iron), alpha-1 antitrypsin (AAT) deficiency, and Wilson disease (copper accumulation). In such cases, patients’ livers are weakened, or have nearly stopped working altogether. How are these facts of any support for evolution? If a mutation occurred in an animal with a ‘primitive’ liver, how could that improve the liver’s functioning, especially considering the complexity and integrated nature of liver function in the context of other body systems? A conceivable improvement might be a more rapid digestion of incoming nutrients than what is currently achieved, but such enhancement would not be without trade-offs. Another improvement might be achieving the same with fewer resources (e.g. blood-flow).

Irreducible complexity

Besides glucose concentration, the liver also manages the level of vital nutrients in the blood, such as other carbohydrates and proteins. The way the liver keeps the latter in check is quite ingenious and irreducibly complex, using gated transport. The three main players are a gate in the cell membrane, a chemical sensor, and proteins labelled with an identification tag. When a protein approaches a gate, the sensor checks the ID tag to determine if the protein may pass, and if so, the gate is opened. If any of these three parts (gate, sensor, tag) is missing, the system fails, and proteins cannot be transported to the right location. If there is no gate, the protein cannot enter or leave the cell, because it cannot go through the cell membrane. If there is no sensor, then the tag cannot be read, and the gate will not be instructed to open. If the protein does not have an ID tag, it cannot be determined whether the protein should be allowed to enter or leave. All three (gate, sensor, tag) would have to evolve and be in place at the same time, or the system would not work, and the creature dies.¹¹ “The liver’s diverse functions and interactions with other organs accentuate the point that homeostasis requires the coordinated action of several body systems [emphasis added]”.¹

Conclusions

The liver plays a crucial role in the human body. Not only is it included in the digestive system, but it also has important functions that affect other systems. This implies that a gradual evolution of the liver is out of the question. Either the interaction with the rest of the body parts was in place from the beginning, or it would not have come into existence at all, since this interdependency is irreducibly complex.

The evidence fits the creationist worldview much better, as deterioration in livers is apparent, but improvements on healthy ones is not.

The liver is essential for life. Without a liver, death ensues very quickly (Proverbs 7:23).

Posted on homepage: 24 January 2025

References and notes

1. Campbell, N. and Reece, J., Biology, Benjamin Cummings, San Francisco, 2002. Return to text.
2. The biogenesis and assembly of the human ATP synthase, Medical Research Council Mitochondrial Biology Unit (Walker group), accessed 8 Aug 2023. Return to text.
3. Kirsch, R., Protein Synthesis; in: Csomós, G. and Thaler, H. (Eds.), Clinical Hepatology, Springer, Berlin, Heidelberg, 1983 | doi:10.1007/978-3642-68748-8_7. Return to text.
4. The EH40 (Health and Safety Executive, UK, 2005) indicates that a long-term exposure (limit of 8 hours average; LTEL) to ammonia should not exceed 25 ppm (parts per million). This is the concentration in ambient air. For comparison, the LTEL for carbon dioxide (CO2) is 5,000 ppm. Health and Safety Executive, EH40/2005 Workplace exposure limits, accessed 20 Jul 2023. Return to text.
5. Hundt, M. et al., Physiology, Bile Secretion, StatPearls Publishing, Treasure island, FL, 2022. Return to text.
6. Liver: Anatomy and Functions, Johns Hopkins Medicine, accessed 27 Jul 2023. Return to text.
7. Delgado-Coello, B., Liver regeneration observed across the different classes of vertebrates from an evolutionary perspective, Cell Heliyon 7(3):E06449, Mar 2021. Return to text.
8. Odokuma, E. and Omokaro, E., Comparative histologic anatomy of vertebrate liver, Annals of Bioanthropology 3(1):1–5, 2015. Return to text.
9. Kent, G. and Carr R., Comparative Anatomy of the Vertebrates, McGraw-Hill, New York, p. 288, 2001. Return to text.
10. Subbotin, V., Arguments on the origin of the vertebrate liver and the Amphioxus hepatic diverticulum: a hypothesis on evolutionary novelties, Pisma v Vavilovskii Zhurnal, 2017. Return to text.
11. Gillen, A., Sherwin, F. and Knowles, A., The Human Body: an intelligent design, Creation Research Society Books, USA, 2001. Return to text.
12. Sanford, J., Genetic Entropy & the Mystery of the Genome, FMS Publications, Waterloo, NY, 2005. Return to text.
13. Spetner, L., Not by Chance! Shattering the modern theory of evolution, The Judaica Press, Brooklyn, NY, 1997; Carter, R.W., Can mutations create new information? J. Creation 25(2):92–98, 2011. Return to text.