The English corner: Gerson therapy analyzed and somewhat criticized

The English corner: Gerson therapy analyzed and somewhat criticized
Cancer Prevention with Nutrition and Lifestyle
The therapy is intended to “detoxify” the body while building up the immune system and raising the level of potassium in cells. The liver is the central organism to help. Toxins must be evacuated from the blood circulation thanks to coffee enema in order to relieve the liver. Supplement are brought to optimize enzymatic and thyroid functions.
The regimen should have total control of everything that enters and leaves the body is the governing principle of the therapy.
No fat except twice one teaspoon a day (for vitamin A) and no meat during the initial phase of 6 weeks. (3)
The vegetables and fruits used on the diet are very high in potassium and very low in sodium. A freshly vegetable juice with organic fruits is brought every hour during 13 hours. (4)
Sources and References
1. USA National Cancer Institute.
The regimen is empirically based on observations made by Max Gerson, M.D., in his clinical practice and on his knowledge of research in cell biology at the time (1930s–1950s).
Few clinical studies of the Gerson therapy are found in the medical literature.
2. The Gerson therapy is rooted in the belief that cancer is a disease of the whole organism, the tumor being only a symptom of a diseased body. Gerson considered cancer to be an accumulation of several damaging factors that combine to cause the deterioration of the entire metabolic system. The goal of the Gerson therapy is to bring the body back to its normal metabolic state, or as near to this state as possible, and to keep the metabolism in natural equilibrium.[[Vous devez être inscrit et connecté pour voir ce lien],[Vous devez être inscrit et connecté pour voir ce lien]]
3. Gerson C, Walker M: The Gerson Therapy: The Amazing Nutritional Program for Cancer and Other Illnesses. Kensington Publishing Corp, 2001.
NB: However, this restriction may continue through the entire course of the therapy, depending on the individual patient. Some changes in the original diet have occurred over time, 
4. Taking specific vitamin and mineral supplements plus pancreatic enzymes is the second component of the regimen. Although there have been additions and substitutions to the basic list of supplements, there have been few changes since the 1940s. The typical range of supplements includes the following:
[list=margin-top][*]Potassium solution
[*]Lugol’s solution (potassium iodide, [Vous devez être inscrit et connecté pour voir ce lien], water)
[*]Coenzyme Q10 and vitamin B12 (substitution for injectable crude liver extract, no longer used).
[*]Vitamins A, C, and B3 (niacin)
[*]Flaxseed oil
[*]Pancreatic enzymes (to assist in the digestion and the elimination of the breakdown products in the colon)
[*]Pepsin
[/list]
The potassium solution (potassium dissolved in water) is to help increase the ratio of potassium to sodium in the cells. Lugol’s solution, which consists of 5 g of iodine and 10 g of potassium iodide dissolved in water, is given to increase the body’s metabolic rate. The potassium solution and Lugol’s solution are both added to the hourly juice intake.[[Vous devez être inscrit et connecté pour voir ce lien]-[Vous devez être inscrit et connecté pour voir ce lien]]

Preamble to discussion
I’m not a physician nor a biologist. I don’t recommend anyone to think that I advise to follow the Gerson diet without using their own common sense and / or assistance from a recognized graduated physician.
We must be conscious that whenever we take off one ingredient from the whole Gerson therapy, we unbalance the diet. There is a balance to find, deficiencies to fill. We do not necessarily perceive what this implies by subtracting a parameter.
However, I’m going to give my perception of some elements. See the contraindication here!
Perceive, think & act
            The central commander is the liver, helped by the thyroid, in this electrical and chemical disorder. When taking juices with fruits, vegetables and supplements, a die-off will most likely take place (health crisis or Herxheimer crisis), since our enzymes are then mainly available to deal with metabolism and far less for digestion. We should be well-informed to deal with.
As a consequence, the body receive the time, the opportunity and the capacity to get rid of dysfunctional cells and toxins stored in fat tissue.
In most cases people die from cachexia – not directly from cancer –, a liver overburdened and lack of useful nutrients to balance homeostasis because our liver is no longer able to proceed in an adapted way.
The liver is more than the chief foreman. The liver is the traffic light at the crossroads in rush hour.
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Wisdom consists in using, when it is necessary, some spirit; and whenever it is necessary to use it, instinct. It is therefore a matter of sensitivity – of a certain sensitivity which perceives and provides for the balance of these two powers.
Paul Valéry

Mettre tout en équilibre, c'est bien. Mettre tout en harmonie, c'est mieux.
=> “Bringing everything in balance is good. Putting everything in harmony is better”.
Victor Hugo.

To be continued.

Potassium solution
Gerson wrote in 1958:  “Cancer is not a single cellular problem: It is an accumulation of numerous damaging factors combined in deteriorating the whole metabolism, after the liver has been progressively impaired in its functions.”
Harmony must reign to recover. Harmony obeys to the totality law. We must preserve balance in the environment of the cells. It implies that we shouldn’t modify the mineral metabolism with drugs. Otherwise it’s going to overburden the liver work.
The two main essential minerals inside and outside the cell are sodium and potassium.
According to Dr. Gerson, people with cancer also have too much sodium and too little potassium in the cells in their bodies, which causes tissue damage and weakened organs. The goal of the Gerson therapy is to restore the body to health by repairing the liver and returning the metabolism to its normal state.
The high potassium, low sodium diet of the Gerson cancer therapy
From Physiol Chem Phys. 1978;10(5):465-8. F W Cope. PMID: 751080
Abstract
“The high potassium, low sodium diet of the Gerson therapy has been observed experimentally to cure many cases of advanced cancer in man, but the reason was not clear. Recent studies from the laboratory of Ling indicate that high potassium, low sodium environments can partially return damaged cell proteins to their normal undamaged configuration. Therefore, the damage in other tissues, induced by toxins and breakdown products from the cancer, is probably partly repaired by the Gerson therapy through this mechanism.”
Electrolyte imbalance
There are many potential causes of electrolyte derangements in cancer patients …
*) For further reading and having a 2-sides view
- Unproven methods of cancer management – Gerson method.
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- The cure of advanced cancer by diet therapy: a summary of 30 years of clinical experimentation. August 5, 2016. By knoxweb.
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The liver plays the important role. It eliminates the toxins from the body, prepares them so they can enter into the bile ducts, and can thus be eliminated with the bile — that is not an easy job. The most important first step is the detoxification.
- Surviving against all Odds: Analysis of 6 Case Studies of Patients with Cancer who Followed the Gerson Therapy
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Although dietary measures may be helpful in preventing certain cancers, there is no scientific evidence that any nutritionally related regimen is appropriate as a primary treatment for cancer.
Hence, the present case review study of 6 patients with metastatic cancer who used the Gerson therapy aims at critically evaluating each case to derive some valid interpretations of its potential effect.

Potassium channels in cancer therapy
[Vous devez être inscrit et connecté pour voir ce lien] : New targets in cancer therapy
By Antonio Felipe PhD et al. 2006 Elsevier 
Highlights
·      Potassium channels (KCh) are involved in many physiological functions.
·      KCh conduct the flux of potassium ions through the membranes of virtually all-living cells and generate either inward or outward currents.
·      Cells require KCh to proliferate (in normal cycle but also in dysfunctional cancer cells)
·      KCh may play a dual role in cancer progression when there is an altered expression.
·      Impaired expression of KCh has been detected in a number of cancer and tumour cells.
·      K+ channels effectors may partially reverse the MDR phenotype. (MDR cells = Multiple Drugs Resistant cells).
·      A large body of data indicates that tumour cells up-regulate KCh when undergoing dedifferentiation.
·      It has been shown that induction of KCh triggers enough hyperpolarization to promote the exit of Ca2+ from internal reservoirs and to activate plasma membrane Ca2+ channels (CRAC channels).
·      Currently, there is no broad consensus on the role of KCh in cancer, except that KCh could be used as a conveyor to target tumor cells in channelopathies.
Abstract Background:
Potassium channels (KCh) are the most diverse and ubiquitous class of ion channels. KCh control membrane potential and contribute to nerve and cardiac action potentials and neurotransmitter release. KCh are also involved in insulin release, differentiation, activation, proliferation, apoptosis, and several other physiological functions. The aim of this review is to provide an updated overview of the KCh role during the cell growth. Their potential use as pharmacological targets in cancer therapies is also discussed. Methods: We searched PubMed (up to 2005) and identified relevant articles. Reprints were mainly obtained by on line subscription. Additional sources were identified through cross-referencing and obtained from Library services.
Results: KCh are responsible for some neurological and cardiovascular diseases and for a new medical discipline, channelopathies. Their role in congenital deafness, multiple sclerosis, episodic ataxia, LQT syndrome and diabetes has been proven. Furthermore, a large body of information suggests that KCh play a role in the cell cycle progression, and it is now accepted that cells require KCh to proliferate. Thus, KCh expression has been studied in a number of tumours and cancer cells.
Conclusions: Cancer is far from being considered a channelopathy. However, it seems appropriate to take into account the involvement of KCh in cancer progression and pathology when developing new strategies for cancer therapy.
Vocabulary: Channelopathy
Channelopathies are a group of diseases caused by the dysfunction of ion channel subunits or their interacting proteins. These diseases can be inherited or acquired by other disorders, drugs, or toxins. Mutations in genes encoding ion channels, which impair channel function, are the most common causes of channelopathies.
Cell cycle and proliferation, cell migration, invasion and apoptosis are all processes that can be modified by the expression of potassium channels.
1. Introduction
Cancer is a multifactor process that involves several temporal steps. Cells first acquire a phenotype through the altered expression of proteins and genes. Afterwards, tumour cells proliferate massively and do not undergo apoptosis. Chemotherapy and radio-sensitization have been widely used to block this progression. However, the use of these therapies is not synonymous with success. Nucleoside analogues have been widely used as a first attempt to control the cell cycle. These molecules are taken up by the cells by means of membrane transport systems. (…)
Although a lot of effort is involved in designing individual treatments, most current strategies are not selective. They may be harmful and are sometimes unsuccessful. (…)
Novel technologies such as genomics and proteomics have increased the number of human genes known to be differentially expressed in normal and malignant tissues. We have entered a new era, leaving cytotoxic approaches behind to focus on mechanisms based on gene therapy and pharmacogenomics. This new perspective has produced a large body of evidence indicating that KCh could play a relevant role in cancer therapy. Targeting potassium channels for cancer therapy could give rise to successful strategies for the following reasons:
a) KCh are involved in cell proliferation as they control cell cycle progression.
b) KCh show cell and tissue-specific expression.
c) These proteins are highly sensitive to synthetic blockers and natural peptides, leading pharmaceutical companies to design more effective and selective molecules.
d) Current therapies for nerve and cardiac diseases successfully target KCh and have few side effects.
e) Impaired expression of KCh has been detected in a number of cancer and tumour cells.
In addition, overexpression of KCh has been described in some MDR cell lines and K+ channels effectors may partially reverse the MDR phenotype [7]. Furthermore, KCh control upstream nucleoside derivative uptake pathways [9]. Therefore, a combination of therapies involving chemotherapeutic agents and K+ channels blockers has been proposed.
MDR cell lines = Multiple Drug Resistant Cells.
2. Method (….)
3. Results
3.1. Criteria for the selection of studies (…)
3.2. Potassium channels
Potassium channels are one of the most diverse classes of membrane proteins. They have more than 75 different genes. KCh conduct the flux of potassium ions through the membranes of virtually all-living cells and generate either inward or outward currents. For an exhaustive description of their activities and structures, refer to the classical handbook on ion channels by Hille [10].
3.3. Potassium channels and cell proliferation
Pharmacological tools have opened the way to understanding the role of K+ channels in cell proliferation. Experimental evidence in cellular physiology and pharmacology demonstrates that KCh are involved in the proliferation of normal and tumour cells. The physiological role of K+ channels in cell growth has been confirmed by a number of experiments. In such experiments the number of normal or tumour cells diminished when K+ channels were blocked with toxins or drugs.
(…) No direct evidence of the mechanism has been provided. (…)
There are several hypotheses that could explain the KCh control of the cell cycle. The soundest of these involves Ca2+ signaling. Calcium is important in cell physiology. Certain thresholds are crucial to promoting or inhibiting several signal transduction pathways [24]. During lymphocyte proliferation, it has been shown that induction of KCh triggers enough hyperpolarization to promote the exit of Ca2+ from internal reservoirs and to activate plasma membrane Ca2+ channels (CRAC channels) [25]. The CRAC channels are voltage-independent, so they do not close at hyperpolarizing membrane potentials as normal voltage-gated Ca2+ channels do and exhibit a pronounced inward rectification, which promotes Ca2+ influx from the extracellular medium. This intracellular rise in Ca2+ initiates appropriate signaling, leading to lymphocyte activation and proliferation. Intracellular Ca2+ activates calcineurin leading to NF-AT (nuclear factor of activated T cells) dephosphorylation. NF-AT accumulates into the nucleus and binds to the promoter element of the interleukin 2 gene (IL-2) triggering IL-2 production and T-cell activation [25]. Three types of KCh are involved in this process in immune system cells: Ca2+ dependent K+ channels (KCa3.1); voltage-dependent K+ channels (Kv1.3) and inward rectifier potassium channels (Kir2.1), [7,12,13,15,16,24–28]. (…)
On the other hand, experimental evidence indicates that several membrane potential changes occur during cell growth. Highly proliferating cells are more depolarized than normal or quiescent cells [38–40]. This is an intriguing situation, as KCh mostly generate hyperpolarization by extrusion of K+ from the cell. However, during the first phases of the cell cycle – G1 or G1/S transition – partial hyperpolarization as a result of KCh, and Kv in particular, may be needed [13,24]. A rational explanation would be that KCh are needed to control a specific check point during these stages.
Proliferation also involves changes in the cell size and KCh may be involved contributing to the regulatory volume control during the cell cycle. Several studies indicate that KCh contribute to cell volume control [41,42]. This is because KCh are involved in K+ transport across the cell membrane, and ion movements, mainly K+ and Cl- , are related to water homeostasis. In fact, a relation between KCh and aquaporin expression has been pointed out during cell differentiation [43,44]. Inhibition of KCh by blockers such as TEA, 4-AP and Cs+ increased cell volume and decreased the rate of cell proliferation [41,42]. However, this scenario highlights some apparent contradictions. Proliferation and apoptosis are opposite events but both involve KCh activation. Whilst experimental data indicate that proliferation is fully inhibited when cell volume increases, cell shrinkage is one of the hallmarks of apoptosis. Intracellular K+ and Cl- efflux accompanying water efflux and cell shrinkage triggers a reduction in cytosolic K+ and relief of apoptotic inhibition. This loss of intracellular ions also plays a primary role in caspase activation and nuclease activity during apoptosis. These evidences lead researches to suggest a dual role for KCh during cell growth and apoptotic death. In this context, whilst macrophage proliferation activates Kv1.3 and Kir2.1 channels, LPS- and TNF-a-induced activation, both triggering apoptosis, increases Kv1.3 and abrogates Kir2.1 [16,17]. In summary, there is no clear consensus as to where KCh exert their specific control on cell cycle progression. However, the bottom line is that the pharmacological treatment of cells with KCh inhibitors impairs cell growth.
3.4. Potassium channels in tumour and cancer cells
Besides the role of KCh during cell growth, highly proliferating cancer cells either up- or down-regulate KCh. Furthermore, the expression of KCh is impaired in several types of tumours. It has been demonstrated that a certain grade of malignancy correlates with the expression of KCh. Although several types of KCh have been associated with a highly proliferative state only a few types have clearly oncogenic effects. Thus, only Kv10.1 and K2p9.1 generate oncogenic phenotypes when introduced in healthy animals [45–47]. Altered expression of members from all groups of KCh has been found in different types of tumours and cancer cells. Whilst Kv1.3 is the most documented of the Kv1 (Shaker) family and it is overexpressed in breast, colon and prostate cancer, Kv1.1 and Kv1.5 show impaired expression in breast and glioma malignant cell lines, respectively. Recently, an increase of Kv7.1 (KCNQ1) and KCNE1 subunits has been detected in germinal tumours [43]. Besides the oncogenic properties of Kv10.1 (see above), members from Kv10 (eag) and Kv11 (erg) families are expressed in a number of tumour and cancer cell lines. Thus, Kv10.1–2 were expressed in breast and neuroblastoma cancer and Kv11.1 has been detected in gastrointestinal, endometrial, neuroblastoma and leukemic cancer and cell lines. In addition, several inward-rectifier potassium channels (Kir) have been also detected in tumours. An increase of Kir proteins has been described in breast and lung cancers. However, in glioma, whilst Kir2.1 expression is inversely correlated with malignancy, an increased expression of Kir4.1 has been documented. The expression of KCa1.1 (BK) and KCa3.1 (IK) is also abundant in neuroblastoma and prostate cancer. Finally, altered expression of K2p9.1 has been observed in breast and lung cancers which correlate with malignancy in cell lines. Two factors may be involved in the impaired expression and role of KCh during cancer: cytokines and dedifferentiation. Studies in animal models have shown that several cytokines, including tumour necrosis factor-a (TNF-a), interleukin-1 (IL-1), IL-6 and interferon-g (IFN-g), among others, can produce signs, symptoms and biochemical features that are commonly observed during cancer [48]. Functionally, cytokines are classified as either pro-inflammatory or anti-inflammatory. These compounds may act synergistically, or counteract, resulting in an effect that is significantly different to the sum of the individual effect. Cytokines exhibit pleiotropy and redundancy. Thus some functions can be mimicked in part by other cytokines [49]. These features have been partially demonstrated in the case of TNF-a [48]. As a result of a systemic inflammatory response, KCh expression may be regulated by TNF-a dependent and independent mechanisms [16,17,50,51]. Clinical studies have demonstrated elevated circulating TNF-a levels in cancer patients as well as in other inflammatory diseases [52]. This cytokine is generated by leukocytes in response to an insult, such as an infection, AIDS or cancer [48,52]. However, while the expression of KCh may be increased in tumours, these proteins are downregulated in other tissues under this systemic response [50,51]. A rational explanation could be given on the basis of the balance of pro- and anti-apoptotic cytokines that may also contribute to different cellular responses [49]. Another conflictive issue could be raised as a result of the cellular dedifferentiation generated by cell growth. As a result of a neoplastic process, cells proliferate but concomitantly become dedifferentiated. These two processes are related and the interpretation of data is difficult. Recently, an increasing amount of evidence has been obtained [53–55]. Currently, there is no broad consensus on the role of KCh in cancer. However, evidence that tumour cell invasion can be handicapped by the use of channel blockers points towards the involvement of KCh in cancer progression and pathology. A summary of the data collected to date for neoplastic cells and tumours is presented in Table 3. These are just a few examples from an ever-growing list.
4. Conclusions
Potassium channels (KCh) in cell membranes regulate cellular excitability and proliferation. The central role of these ion channels in cell function has made them the target of several channelopathies. In light of the increasing amount of evidence showing that KCh are involved in cell proliferation and tumour growth, it seems that these proteins could be considered a pharmacological tool during cancer progression and pathology. The persistence of the MDR phenotype handicaps the treatment and the successful use of chemotherapy and radio-sensitivity. Therefore, novel strategies based on a new post-genomic era should be considered. In fact, the use of KCh proteins in combination with other therapies could improve therapy strategies. The use of ion channels as therapeutic targets during cancer is not exclusively designed to halt cell growth. In addition, these proteins have been also proposed as effective targets for cancer pain [56]. Furthermore, a large body of data indicates that tumour cells up-regulate KCh when undergoing dedifferentiation. This fact may also suggest that these proteins can be used as tumour markers. In conclusion, although cancer is far from being considered a channelopathy, the latest literature indicates that the time has come to consider potassium channels in anticancer therapies and to undertake organized studies.
Vocabulary:
*) KCh = potassium channel. Ion transport molecules are involved in many physiological and pathological processes.
*) Ion = an atom or molecule with a net electric charge. 
*) Channelopathy
Channelopathies are a group of diseases caused by the dysfunction of ion channel subunits or their interacting proteins. These diseases can be inherited or acquired by other disorders, drugs, or toxins. Mutations in genes encoding ion channels, which impair channel function, are the most common causes of channelopathies.
Cell cycle and proliferation, cell migration, invasion and apoptosis are all processes that can be modified by the expression of potassium channels.
*) MDR
MDR phenotype = type of cells that is MDR. MDR = Multiple Drug Resistant.

Inductive reasoning about potassium
In general, a person who uses this type of reasoning starts from one or more observations and then leads to a conclusion. There can therefore be a hiatus in the conclusion if one of my sources is "conservative" (reluctant to change), or if I haven’t caught an element during research. It is obvious that potassium plays a key role in the ionic balance of the cell. Cancer or not. Everyone agrees on this.
Attempt by a Boeotian to explain the duality of potassium
Here we must distinguish the case of prevention from the case of propagation. In the event of a cell reached by the crab, potassium will use the ion channels (KCh) to penetrate the cell. Potassic channels (KCh) play a role in cell growth. It therefore seems appropriate to take into account the involvement of KCh in the pathology and the progression of cancer and in the development of new cancer treatment strategies.
I’m not telling you that it’s contraindicated / inappropriate: We don’t know how and precisely when. It's a possibility. Malignant cells could use the potassium channels to make a path and expand more easily. There, it would be necessary to change your approach. Prevent the malignant cell from stinging the fuel from its healthy sisters. But that's another subject.

Why and how much iodine do we need?
Part I: Global point of view about energy levels
Part II: High supplement iodine in the case of cancer
Part III: Metabolism of iodine – How much iodine potassium is absorbed?
We have to make the difference between iodine coming from supplement from iodine coming from foodstuff. Iodine is useful for thyroid as a cofactor. If you eat fish and drink milk, you aren’t supposed to lack iodine (RDA target).
Iodine is an essential trace mineral. The thyroid gland manufactures thyroid hormone from iodine and tyrosine. Iodine needed to make thyroid hormones, which regulate metabolism and the body's ability to burn carbohydrates and fats for energy. Thyroid hormones stimulate our basal metabolic rate (BMR). Iodine is also required for optimal immune function.
[Vous devez être inscrit et connecté pour voir ce lien], the body requires 150 to 200 mcg of iodine, with as much as 80% of these going to the thyroid. But pregnant and lactating women need more (220 – 290 mcg) (according to RDA).
doi: [Vous devez être inscrit et connecté pour voir ce lien]
Iodine helps maintaining optimal energy levels
Iodine plays a vital role in maintaining optimal energy levels of the body by the utilization of calories, without allowing them to be deposited as excess fat.
We’re not talking about deficiency in iodine (leading to infant cretinism) but about a lack of (pharmacological dose).
Iodine – The Mineral that Charges your Energy Battery
Sluggish thyroid function leads to a low metabolic rate with consequent easy weight gain and fatigue. Iodine is found in every cell of the body, so it likely has far broader roles (2) in maintaining health. Iodine is used up much when there is increased risk of infections – both viral and bacterial. Or with low-grade infection. For instance, with IBS or gingivitis.
The body's ability to resist infection and disease is hindered by long-term deficiency of essential minerals including iodine, zinc and selenium. (1)
How Does It Work?
Iodine's biological functions are best understood in terms of thyroid function. The pituitary gland secretes thyroid-stimulating hormone (TSH), which stimulates the recovery of iodine from the blood and orchestrates the use of iodine in thyroid hormones. In turn, the thyroid gland makes thyroxine (T4), which contains four iodine atoms. The iodine-containing enzyme deiodinase converts T4 to triiodothyronine (T3), which contains three iodine atoms and is the most active thyroid hormone. When thyroid hormone levels are extremely low, the pituitary increases its secretion of TSH, which leads to an increased risk of goiter. (3)
Selenium is also involved in making thyroid hormones, and a lack of selenium exacerbates iodine deficiency. The two minerals by themselves may not increase thyroid activity, but they should be included in any treatment for low thyroid activity. Basic trace elements used by thyroid are Zn, Mg, Se and I.
Note that tap water contains fluoride and chlorine, which could inhibit the absorption of iodine in already poor situations.
Sources and References
1. Iodine – The Mineral That Charges Your Energy Battery
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2. Risks factor linked to iodine deficiency                    
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3. By Jack Challem, aka “The Nutrition Reporter”[Vous devez être inscrit et connecté pour voir ce lien]
If we lack Iodine, Brome, Chloris and / or Fluor can squat the place (same family: halogens => Pollution by halogens).
4. Optimal amount of daily I intake that will result in the greatest mental and physical levels of wellbeing in the majority of a population with a minimal degree of negative effects.
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RDA for iodine in adult men and women is at 150 μg per day.
Minimal accurate intake: 225 mcg.
Optimal intake (no infection): 1 000 mcg (with staples every 10 days).
Estimated daily intake of Japanese is averaging 5.3 mg (*), in the non-coastal areas of Japan. This relatively low I intake, by Japanese standard, is more than 30 times the recommended daily amount of I in North America and Europe.
*) Cann S., Netten J., Netten C., Hypothesis: Iodine, selenium and the development of breast cancer, Cancer Causes and Control 11:121-127, 2000.
Eating much cruciferous often could block iodine absorption (Brussel sprouts, cauliflower, broccoli, radishes, turnips, kale, and watercress).
5. “You, me and Iodine” (part two)
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Lisa FITZGIBBONis a naturopath and medical Herbalist (Bachelor of Health Science degree (Complementary Medicine). And, I’ve been a qualified health practitioner for the last twelve years of that time.
Interesting links
1. Why the hype on thyrotoxicosis of inorganic iodide?
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- How much iodine do we need?
- Wolff-Chaikoff Effect.
-  Absorption of iodine. The absorption of iodine is different depending on whether it is organic or synthetic.
- Endocrine disruptors (Fluorine, chlorine and bromine).
- Histaminose and iodine.
- Potassium iodine and iodide.
- RDA for iodine and iodine in foodstuff.
- Roles of iodine in metabolism
- Take care of your thyroid - Alternative Santé. (Potassium iodide bounds to thyroglobulin and blocks the operation of the gland because of antibodies).
- Auto-regulatory reduction in the synthesis and secretion of thyroid hormones following the ingestion of a large amount of iodine. The suppressive effect may persist by the weak functioning of thyroid.
- Start selenium first before iodine supplementation!
- Excess of an iodine contribution and progressive dosage to take into account.
- Higher dose in the event of a detox
2. Lugol solution (5% iodine and 10% potassium iodide) (or a 1/2 ratio)
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Lugol solution: 1 drop contains 8 mg of iodine.
Note: We shouldn’t take more than 1 mg iodine and that’s a very high amount. Except if your purpose is to use a machine-gun to target the crab with a high level of antioxidants, hoping that the liver will support the release of LPS residues, and evacuated toxins thanks to a strict diet based on improved fruit juices.  See the second part for more explanation.
3. Take vitamin C away from iodine (half an hour away from iodine)
They work in different ways and combining them reduces the effectiveness of both.
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NB: It is necessary to distinguish the concomitant contribution and the availability of nutrients. Zoëlho advises the association between Se, Mg, Vit C and I. Probably because they are cofactors to form thyroxine (T4) and triiodothyronine (T3).
But potassium iodide is a supplement in the form of an alkalizing salt and an antioxidant (ability to neutralize ROS). Vitamin C being an acid, its effectiveness will be reduced in the presence of a basic molecule (potassium is a base). Like when we associate baking soda with vitamin C or Coca-Cola. Less likely for iodine to be efficient, so.
4. Benefits of Iodine on Thyroid Health - Iodine Interactions
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5. Lithium-based treatment (mood regulator) can increase the need by iodine by altering the release of T3 and T4 hormones by the thyroid gland.
Source : A. Martin et al. Apports nutritionnels conseillés pour la population française. Ed Lavoisier, Tec & Doc. 2001.
6. List of MD to determine how much iodine you may dose
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7. [url=https://books.google.fr/books?id=V0PHDwAAQBAJ&pg=PA205&lpg=PA205&dq=does+vitamin+c+neutralize+iodine+supplement&source=bl&ots=-SINbYBMmI&sig=ACfU3U1dMlrVpAjpViyq7AUAL2A8gRnl2w&hl=fr&sa=X&ved=2ahUKEwiymuSDoJ_nAhVNCewKHeLaB1w4ChDoATAGegQIDBAB#v=onepage&q=does vitamin c neutralize iodine]Do not take iodine supplement with cancer: [/url]Iodine neutralize ROS.
Neutralizing ROS can actually protect cancer cells from apoptosis.
8. Can light therapy play a role in prevention and treatment of thyroid/low metabolism problems?
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Part II: High supplement iodine in the case of cancer
Dual role of iodine in cancer therapy
We are not talking about supplementing to overcome a lack / a deficiency. But to use high dose iodine as anti-ROS and stimulant for the thyroid. 30% of the global population is iodine deficient but it depends much on where you live and where your food comes from.
ROS = Reactive Oxygen Species.
We have here to consider how high dose iodine is going to affect the proliferation, apoptosis, and migration ability of cancer cells.
In addition to functioning as an antioxidant, anti-inflammatory, and anti-proliferative agent, we are going to see how iodine has also the ability to induce apoptosis and differentiation in cancer cells.
Note that free iodine is unstable in water.  Iodine must be linked to another electron to be stable.  When stored in water, iodine can readily dissolve and can potentially react with other substances in the water, leading to a loss of potency. Iodine has a very low solubility in water because it is non-polar. (Any molecule consisting of two identical atoms is non-polar, since the electro-negativities of the atoms are equal.) (See the link / video “2. Iodine vs Iodide vs Molecular Iodine” for a more comprehensive explanation).
Taking iodine supplement must be strictly progressive. Excess iodine can cause heart failure through hyperthyroid and hypothyroid states. Oral potassium iodide and Lugol's iodine have been reported as successful treatments [[Vous devez être inscrit et connecté pour voir ce lien]]. However, if iodine therapy is not administered or monitored correctly, serious morbidity can result. Lugol’s iodine is poorly absorbed. Lugol is a solution of [Vous devez être inscrit et connecté pour voir ce lien] with [Vous devez être inscrit et connecté pour voir ce lien] in water (to improve the suspension of iodine in water).
Iodine is more soluble in potassium iodide solution due to the formation of a complex ion. When iodine is added to a solution of potassium iodide, the following equilibrium is established: 
I2 + I- ⇌ I3- The triiodide ion (I3-) formed in the solution increases the solubility of iodine by forming a complex with it. This complex formation reduces the concentration of free iodine in the solution, thereby increasing its solubility.
In this [Vous devez être inscrit et connecté pour voir ce lien] high iodine levels inhibited cell proliferation and promoted apoptosis and migration of PTC cells. (PTC = Papillary thyroid carcinoma = endocrine tumor).
The levels of autophagy and apoptosis in PTC cancer tissues, and activities of BRAF kinase in peripheral blood increased with increasing levels of iodine. At high iodine levels, the proliferation rate decreased, and apoptosis percentage and migration rates increased compared with the no-iodine group.
Useful links
1. Curious About Iodine, & 3: Antioxidant, Immune Support, Anti-Cancer
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Iodide functions as an antioxidant through its action as an electron donor when it interacts with peroxidase enzymes ([Vous devez être inscrit et connecté pour voir ce lien]). In its role as an electron donor, iodide can neutralize reactive oxygen species (ROS) and prevent lipid peroxidation of cell membranes. 
While the body has several endogenous systems to address oxidative stress, mineral antioxidants play an important role in electron transfer and in redox chemical reactions in the tissues where they concentrate. Overall, iodine has been shown to have a favorable impact on total serum antioxidant status ([Vous devez être inscrit et connecté pour voir ce lien]).
Iodine and the immune system
Iodine can support the innate immune system to fight bacterial and viral infection and has immunomodulatory effects on immune cells.
Iodine is taken up and metabolized by immune cells where its function as either an anti-inflammatory or pro-inflammatory agent is determined by the physiological context. Iodine can support the innate immune system to fight bacterial and viral infection and has immunomodulatory effects on immune cells. This immune enhancing effect increases expression of cytokines and chemokines that control cell trafficking and regulate the nature of the immune response. Overall, this has the effect of enhancing the immune system’s ability to fight infection while keeping the immune response balanced ([Vous devez être inscrit et connecté pour voir ce lien]).
Phagocytes, granulocytes and monocytes, types of leukocytes cells within the immune system, harbor the highest concentration of iodide transporters. In vitro studies show that iodine induces transcriptional modification in human leukocytes, resulting in the upregulation of genes that promote activation of cytokines and chemokines. The observed transcriptional changes in the leukocytes produced a mix of cytokines that were both pro- and anti-inflammatory, indicating a balanced immune response that can both promote and resolve inflammation ([Vous devez être inscrit et connecté pour voir ce lien]).
Respiratory infections
(…)
Anti-cancer effects of iodine
Iodine concentrates in many extra-thyroidal tissues and has particular anti-tumorigenesis effect in mammary, prostate, pancreas, lung, and nervous system tissue.
In addition to functioning as an antioxidant, anti-inflammatory, and anti-proliferative agent, iodine also has the ability to induce apoptosis and differentiation in cancer cells. The reactive oxygen species of singlet oxygen, superoxide anions, hydrogen peroxide and hydroxyl radials have a wide range of cellular and molecular effects, resulting in mutagenicity, cytotoxicity, and alterations in gene expression. Molecular iodine (I₂) can function as a scavenger and antioxidant that neutralizes various ROS that are known to be cytotoxic and implicated in the development of cancer ([Vous devez être inscrit et connecté pour voir ce lien]).
Molecular iodine (I₂) inhibits cell proliferation and induces apoptosis in cancer cells through a direct mitochondrial effect and an indirect effect through iodolipid generation. Through its oxidant/antioxidant properties, molecular iodine (I₂) can directly dissipate the mitochondrial membrane potential, triggering mitochondrion-mediated apoptosis in cancer cells without affecting the mitochondria of normal tissue ([Vous devez être inscrit et connecté pour voir ce lien]).
Fig 2. Anti-cancer effects of iodine associated with mitochondria and PPAR gamma.
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Credit: Aceves C, Mendieta I, Anguiano B, et al. Molecular iodine has extrathyroidal effects as an
antioxidant, differentiator, and immunomodulator. Int J Mol Sci. 2021; 22(3):1228.
In the presence of high levels of arachidonic acid (AA), molecular iodine (I₂) induces the formation of 6-iodolactone (6-IL), which is an iodinated derivative of AA. AA is a polyunsaturated free fatty acid present in the membrane phospholipid layer of all mammalian cells. Tumors contain a significantly higher concentration of AA, and when treated with molecular iodine (I₂), 6-IL greatly increases. It is proposed that the increase in 6-IL indirectly contributes to the anti-proliferative and apoptotic effect of molecular iodine (I₂) ([Vous devez être inscrit et connecté pour voir ce lien], [Vous devez être inscrit et connecté pour voir ce lien]).
Additionally, 6-IL has a high affinity for peroxisome proliferator-activated receptor gamma (PPARγ). PPARs are nuclear transcription factors that regulate cancer cell proliferation in addition to their classical role in maintaining lipid and glucose homeostasis ([Vous devez être inscrit et connecté pour voir ce lien]). PPARs exist as three substrates, with PPARγ having the highest affinity for IL-6. AA is a natural ligand of PPARs, meaning that it binds readily to this receptor. When molecular iodine (I₂) promotes the formation of 6-IL in the presence of AA, 6-IL will bind to PPARγ with an affinity six times higher than AA. The binding of 6-IL to PPARγ results in a regulating effect on cancer cell proliferation ([Vous devez être inscrit et connecté pour voir ce lien]). In a preliminary clinical study of 22 women with breast cancer, those who received 5 mg/day of molecular iodine (I₂) rather than placebo showed an increase in PPARγ expression, increased apoptosis, and decreased proliferation of cancer cells ([Vous devez être inscrit et connecté pour voir ce lien]).
Iodine and breast health
(…)
Iodine and prostate health
(…)
The dose response effect of iodine in benign and cancerous conditions
Molecular iodine (I₂) is the form of iodine heralded for its antineoplastic effects. Although seaweed contains iodine in several chemical forms, molecular iodine (I₂) is commonly found in seaweed consumed in traditional Asian cultures and used for treatment of breast cancer due to its ability to soften tumors and reduce nodulation ([Vous devez être inscrit et connecté pour voir ce lien]).
Dose response studies in humans demonstrated that iodine supplemented at 1.5 mg/day or less had no effect on benign pathologies whereas, dosages of 3.5 mg/day up to 6 mg/day, mainly in the form of molecular iodine (I₂), exhibited significant beneficial actions on mastalgia and BPH. Dosages at 9 mg/day and 12 mg/day showed the same benefits but had a greater impact on thyroid function and produced a variety of minor side effects ([Vous devez être inscrit et connecté pour voir ce lien], [Vous devez être inscrit et connecté pour voir ce lien]).
In summary
The fact that 30% of the global population is iodine deficient is concerning especially when we consider that iodine has so many functions and concentrates in a variety of tissues. Our need for iodine may be dependent on a number of factors including where we live, what we consume and how much iodine our own body needs to stay sufficient while supporting all of the processes that depend on an adequate amount of iodine.
2. Iodine vs Iodide vs Molecular Iodine (Video 6’)
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When we say Molecular Iodine we are referring to I2. => Molecular structure of an atom and electron prevalence (valence layer = last peripheral layer of electrons).
NB: This short video is fine to perceive how I- links to I2 to form I3-. 
3. I2 in medical uses
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Molecular iodine (I2) is the only species of iodine which represents some therapeutic efficacy in many applied areas.
Synonyms: Molecular iodine, diatomic iodine, free iodine.
3. I2 in seaweed [url=https://ijprajournal.com/issue_dcp/Molecular Iodine (I2) Its Occurrence, uses and safety profile.pdf][Vous devez être inscrit et connecté pour voir ce lien]
Commercially molecular Iodine (I2) is extracted from seaweed in large quantities. From many species of seaweed, the main reservoirs of molecular iodine are brown and red algae.
Molecular iodine (I2) is practically insoluble in water but is very soluble in aqueous solutions of iodides forming the water-soluble ion triiodide (I3-) [7].
=> Mixed solution with I2 and I3-

Part III: Metabolism of iodine – How much iodine potassium is absorbed?
What kind of iodine or iodide in seaweed extract
Seaweed contain large amount of iodine (*1). Therefore it’s advised to take titled supplement made from seaweed / kelp (varech). Iodine may be found in several chemical forms or species, generally characterized as inorganic and organic forms. Iodide (I-) is the most common inorganic form of iodine in brown algae (Küpper et al., 2008), but iodate (IO3-) is sometimes also identified, generally in less quantity (Hou et al., 1997). Iodine can also be organically bound to macromolecules in brown algae (Hou et al., 2000), e.g. with polyphenols.
Sea kelp and seaweed typically contain iodine in the form of potassium iodide. This is the most common form of iodine found in natural sources and is also used in many iodine supplements. 
*1) [url=https://ift.onlinelibrary.wiley.com/doi/10.1111/1541-4337.12918#:~:text=Iodine may be found in,et al.%2C 1997][Vous devez être inscrit et connecté pour voir ce lien][/url]


Bioavailability of iodine
The concept of bioavailability is frequently relevant to discussions of the tolerable amounts of iodine from seaweeds. The bioavailability of iodine is defined as the proportion of iodine that is released from the ingested food, absorbed by the intestine, and brought into circulation. A related term, bio-accessibility, refers to the proportion of iodine that is released during digestion, without assessing further uptake into the body's circulation. Studies of bioavailability and bio-accessibility are necessary to understand how readily iodine from seaweeds is absorbed during digestion. Since some studies have yielded results indicating that the bioavailability of iodine from seaweeds is low (Romarís-Hortas et al., [Vous devez être inscrit et connecté pour voir ce lien]), bioavailability has been used as an argument for allowing a higher daily consumption of iodine from seaweeds (Bak, [Vous devez être inscrit et connecté pour voir ce lien]). However, contradictory results regarding bioavailability have been found in other studies (Aquaron et al., [Vous devez être inscrit et connecté pour voir ce lien]), and an investigation into the various studies assessing the bioavailability of iodine from brown algae is needed to enhance our understanding of which results can and should be trusted during decision-making.

U-Shaped relationship for health purpose
As for most nutrients, there is a U-shaped relationship between the intake of iodine and the risk of adverse health consequences (Laurberg et al., [Vous devez être inscrit et connecté pour voir ce lien]), meaning that both too low intakes and excessively high intakes may lead to negative health impacts. The consequences of severe iodine deficiency are well-documented and may lead to impaired growth and development (Leung, [Vous devez être inscrit et connecté pour voir ce lien]).

Dietary supplements
In dietary supplements, iodine is often present as potassium iodide or sodium iodide [[Vous devez être inscrit et connecté pour voir ce lien]]. Supplements containing kelp, a seaweed that contains iodine, are also available. A small study found that people absorb potassium iodide almost completely (96.4%) [[Vous devez être inscrit et connecté pour voir ce lien]].
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20. National Institutes of Health. [Vous devez être inscrit et connecté pour voir ce lien] 2020.
21. Aquaron R, Delange F, Marchal P, Lognoné V, Ninane L. Bioavailability of seaweed iodine in human beings. Cell Mol Biol (Noisy-le-grand). 2002 Jul;48(5):563-569. [[Vous devez être inscrit et connecté pour voir ce lien]]
=> As a control we studied in a normal man the bioavailability of pure mineral iodine such as potassium iodide which was excellent i.e. 96.4% and of pure organic iodine such as monoiodotyrosine which was a little lower i.e. 80.0%. Iodine bioavailability from two seaweeds was studied by healthy subjects in Marseille and in Brussels. The iodine bioavailability of Gracilaria verrucosa is better than for Laminaria hyperborean. The urinary excretion of iodine is lower in Brussels (Belgium) than in Marseille (France) for the same seaweed because part of the iodine is stored in the thyroid (normal subjects from Brussels present a mild iodine deficiency with a value of 73 microg/day). 

I- as metabolism defense
Iodide (I⁻) metabolism is crucial for the synthesis of thyroid hormones (THs) in the thyroid and the subsequent action of these hormones in the organism. 
Back to chemistry lessons
I (iodine, atom); I- (iodide ion, with negative charge, 1 electron is free, not paired); I2 (neutral molecule); I3- (red one inside two green molecules, on the picture below). The red one has linked twice with one electron from the peripheral layer of green molecule, forming a tri-atom, aka I3-, standing for tri-iodide ion).
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Lugol’s solution contains potassium iodide (KI) and a stoichiometric amount of elemental free iodine (I2), which confers to it varying strengths, the most commonly available from 1% to 5% (solution with 1%, up to 5% iodine). By reacting with the I2, iodine ion (I-) forms a triiodide ion (I3-), which is soluble in water and has its presence revealed by a yellow or brown color according to its low or high concentration in the solution, respectively. (5) Having the essential capability of reacting with glucose chains, a significant amounts of I3- is “ready to work” wherever the glucose chains are stored.
Note: Lugol's solution 5 % consists of 5% iodine and 10% potassium iodide. 
     • original lugol iodine solution 5%, 100 ml
     • Contains a concentration of 5% iodine
     • A drop corresponds to 6.5 mg of iodine
In contrast to malignant non-keratinized epithelial cells, the typical cells contain abundant glycogen, a polymeric biomolecule composed of thousands of linear chains of 8 to 12 glucose units, on average. (6) After Lugol’s solution is sprayed onto stratified squamous epithelium, the intracellular glucose chains coil up, fitting inside the I3- . This reaction soon turns into an absorbing deep dark brown light one, mimicking the “iodine clock reaction” phenomenon and indicating silently (and for a short time) the presence of a well-glycogenated normal epithelium: the longer the glucose chains are, the more intense the color reaction will be. (7)
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See the video below for a more comprehensive model:
Iodine vs Iodide vs Molecular Iodine (Video 6’) [Vous devez être inscrit et connecté pour voir ce lien]

How much iodine potassium is absorbed?
A small study found that people absorb potassium iodide almost completely (96.4%) [21].
21. Aquaron R, Delange F, Marchal P, Lognoné V, Ninane L. Bioavailability of seaweed iodine in human beings. Cell Mol Biol (Noisy-le-grand). 2002 Jul;48(5):563-569. [[Vous devez être inscrit et connecté pour voir ce lien]]
Potassium is intrinsically soluble and quickly dispersed in the luminal water of the upper digestive tract. The small intestine is the primary site of potassium absorption, with approximately 90% of dietary potassium being absorbed by passive diffusion [[Vous devez être inscrit et connecté pour voir ce lien]]. The majority of iodine being excreted through the urine. But in fact, little is known about the bioavailability of potassium, with the majority of work being centered on the assessment of urinary potassium losses after potassium salt supplementation.
29. Demigne C., Sabboh H., Remesy C., Meneton P. Protective effects of high dietary potassium: Nutritional and metabolic aspects. J. Nutr. 2004;134:2903–2906. [[Vous devez être inscrit et connecté pour voir ce lien]] [[Vous devez être inscrit et connecté pour voir ce lien]]
Note the difference between the absorption of potassium molecule alone and potassium iodine when the studies are mentioning a percentage of absorption. It appears that the small intestine is the principal site of absorption in humans and in rats, with RDA doses. Potassium iodide is absorbed through the intestinal tract and the majority is excreted through the urine.
 
Additional info
Absorption of Potassium Iodide from Gastro-Intestinal Tract
Molecular iodine and water soluble iodine salts release the iodide ion in contact with water. Thus, iodine occurs in water in the form of the iodide ion (I-). Molecular iodine as well as water soluble iodine salts are rapidly converted into iodide in the gastrointestinal tract following ingestion and iodide is efficiently absorbed throughout the gastrointestinal tract. Therefore, toxicological effects can be considered together for molecular iodine and water soluble iodine compounds to the extent that these effects are directly mediated by the iodide ion.
This evaluation is limited to consider the toxicity of inorganic salts of the stable iodine isotope (127I) from which the iodide ion can be liberated, as this form is the relevant one in relation to estimation of a health-based quality criterion in drinking water.
All biological actions of iodine in mammals are attributed to the thyroid hormones (T4 and T3) and the synthesis of normal quantities of thyroid hormones requires an adequate intake of iodide. According to the Nordic Nutrition Recommendations (NNR 2004), the recommended daily intake of iodine is 150 μg/day for older children (from 10 years) and adults.
Source: [Vous devez être inscrit et connecté pour voir ce lien]

To be reminded
I2 is unstable in a water solution. I2 must be mixed with potassium iodide in order to form I3-.
Iodine occurs in water sea in the form of the iodide ion (I-).

By reacting with the I2, iodine ion (I-) forms a triiodide ion (I3-), which is soluble in water.

Comment 
If take of high dose iodine, this must be done progressively. Not when the ill-person suffers from cachexia. The body needs energy to get rid of LPS toxins and cancer cells killed by Iodine. Note that only high dose might be efficient (passive diffusion). I underline the word “might”. It’s possible, not guaranteed.
Vocabulary: Cachexia is characterized by weight loss via skeletal muscle and adipose tissue loss.
In the optic of Gerson therapy, malignant cells aren’t allowed to receive alternative fuel from fats. When cells don’t get carbs, they can adapt and use fats from adipocytes or muscles. Scientists think that cancer causes the immune system to release certain chemicals into the blood. This causes inflammation. These chemicals are called cytokines and contribute to the loss of fat and muscle. The chemicals may make your metabolism speed up so that you use up calories faster. Because your body is using up energy faster than it is getting it, you can have severe weight loss. This can happen even if you are eating normally.
Source: Cachexia (wasting syndrome) – Cancer Research UK.
So, if you choose this option, it must be done very strictly, and only if you have sufficient energy for allowing your liver to get rid of residues and discharged heavy metals (HM), previously embedded in fatty mass. Of course, everything must be done to help your liver. Get informed how to deal with die-off (Herxheimer crisis / healing crisis). The same with smoothies. If you don’t like them (not well prepared), you are going to lack calories, and soon after you're going to lose fat and muscles.
Note: You’ll need selenium with HM and mixed vitamin E (toco). Sulfur from food would be a good choice: Garlic and onions – These vegetables contain sulfur, which helps your liver detoxify itself of heavy metals like lead and arsenic.
If the liver becomes overburden, chlorella and charcoal would amalgam the residue. Here is the coffee enema useful: Coffee enema will open the way-off to get rid fast of the toxins.

What’s the hype with keto-diet?
Don’t follow the hype about the sugar-free diet (through keto-diet tendency) as cancer cells are able to adapt themselves.
Carbohydrates and Cancer
Cancer cells require a lot of glucose for energy — more than normal cells. This is because cancer cells metabolize, or break down, sugars using a different and less efficient process than that of normal, healthy cells. Cells typically use oxygen to burn glucose for energy. Because cancer cells grow in excess and become densely packed, however, they often survive in a low-oxygen environment and have adapted to breaking down sugars in the absence of oxygen — a process called anaerobic metabolism. Unfortunately, anaerobic metabolism is much less efficient than breaking down sugars aerobically, or with oxygen. As a result, cancer cells may need as much as 40 times more glucose than normal cells that function with sufficient levels of oxygen to generate the same amount of energy.
Source: [Vous devez être inscrit et connecté pour voir ce lien]
=> Only carbs with useful nutrients, mainly from fruits and vegetables. But not only if moderate from starch (glycemic load), after the first 6 weeks. 
=> If limited access with a low-carb diet (but sufficient to feed the organism), cancer cells will be on survive mode.