The 4th and 5th cycle of the FEC-T chemotherapy protocol

Nivestim, the culprit that gave me cold sweats, stomach cramps, diarrhoea!

Here are my experiences with Taxotere (Docetaxel):

Cycle 4 – 23^rd September 2016

My morning blood counts were fine, and thus, the next chemotherapy session proceeded as scheduled. The pre-medications were given, with the addition of chlorphenamine injection (Piriton) which made me quite groggy. Piriton injection was given together with dexamethasone to mitigate any allergy reaction towards docetaxel (Taxotere®) if any. I was really hoping that Taxotere is going to be better than FEC, because we are talking about single agent infusion as compared with 3 cytotoxic drugs at one go!

I requested for Emend even though my oncologist said I don’t need it! Well, I told him I already felt nauseous before I went for the blood test! Hence, I wasn’t sure if I would be able to cope with Taxotere without Emend! He relented and said ok! I am totally aware that this is not right, but at this point of time, I will do anything for not getting sick! Anything….

Taxotere infusion went well without any untoward incidents (touch wood!). I was feeling absolutely normal for the first 3 days and even went for a walk at the Botanicals Garden on Day 3! My energy level was normal and I thought “hmm….taxotere really gonna be a breeze!” Certainly not wanting to believe what I have read earlier about this super drug!  Luck was not on my side though...my energy level decreases steadily from Day 4 and remained low until Day 9.

As taxotere will be tough on the white blood cells,  3 Nivestim injections  on Day 4, 5 and 6 has to be administered.  A kind senior onconurse taught me how to administer the ready to use syringe on Day 4 at the day ward. It was uneventful but stomach ache and cramps crept in later in the evening which got worse in the next few days.

Day 5 was the worst day I have experienced so far! Right after I injected Nivestim myself at home, I grew weak, had excessive cold sweat and lose consciousness for a short while, all within 5 minutes! I was pretty sure I injected the substance into the subcutaneous tissues and not in the peritoneal cavity! gosh!

Like the cartoon character flattened down to a paper-thin state rolled over by a truck….I have to stay in bed most of the time since that self-administered injection, feeling really thin and weak like a kitten! Surprisingly, despite all that, my appetite remained the same!

I texted my oncologist about my condition rather “immediately” wanting to know if I will be in trouble. Luckily there was nothing to worry about and he told me to drop by the clinic the next day. I literally have to be on the wheelchair as I was too weak to walk to the clinic! Finally, after waiting for 3 hours, the doctor said, “I think you are allergic to Nivestim, I guess you don’t need to take the 3^rd jab today, but you have to come over next week so that we can monitor your blood counts.” For no apparent reason, I turned bright-eyed and bushy-tailed; I stood up with my wobbly legs and walked down the floors without assistance! Good riddance!

Muscle soreness at the spine and neck area came in on Day 4 and lasted for a few days, not too bad as analgesics were not required. I have long suspected that my pain threshold may be abnormal!

The stomach cramps, dear me, came in waves, followed a typical pattern, reaching a peak of agony, eases off and the cycle continued until you pooped! Ok, we are dealing with loose stools here and this lasted until Day 10! Imodium 3 times a day seemed to control the cramps, but toilet visits maintained at least twice or thrice a day!  

Red spots or petechia were observed on both of my hands on Day 3. I noticed my face were flushing red on the same day which lasted for 2-3 days.

Some hairs started to drop by Day 15, slight discoloration on the toe nails were noticed and eyes were slightly dry and I have to use eye drops occasionally. Skin looked a bit patchy on certain days but resolved somehow. No mouth sores or ulcers. 

The most important change I noted was that my fasting blood glucose readings went up to 6.5- 7 mmol/L on certain days. I understood that hyperglycaemia and glucose intolerance is a known side effect of taxotere, and whether this is transient or going to affect me permanently, there is still lack of data to conclude anything at the moment. Anyway, I tried to reduce intake of rice, wheat and high carb food to manage this side effect.

Some days I felt numbness on my hands and feet, especially at night, so I took neurobion (Vit B1, B6 and B12) tablet occasionally, which kind of helped.

Cycle 5 – 14^th October 2016

My white cell count was about 5.0 X 10³/μL which was surprisingly good despite missing the 3^rd jab last cycle! So, the next Taxotere infusion was given as scheduled. Nothing untoward happened, luckily. I was feeling normal and even went to a Japanese restaurant for dinner that night! I knew that was a false sense of security!

This cycle no filgrastim injection was given. I felt fine throughout the first 3 days, and as expected, on Day 4, I somehow woke up with muscle and neck sore, but still manageable without analgesics. Energy went down slightly but I was fine and totally functional! No stomach ache, no cramps and no sick days! Tiredness was there but you feel fine after taking a nap. So, now we know which the devil is!

I went for my 1^st blood test after a week (Day 8) and the white cell count was down to 2.0 X 10³/μL. The doctor prescribed a strong antibiotic (Ciprobay) for a week, although I thought it was unnecessary (I meant….the count was not critical…). As the doc said, “Better safe than sorry!” I was feeling normal and energetic even though the counts were low….

Surprisingly, I developed a delayed “extravasation” (according to the doctor and to my horror!) at the injection site. Itchiness and tiny blisters appearing on the skin but got slightly better after I applied a steroid cream. I was later prescribed with Reparil Gel, which supposedly works best, according to my doc!

Redness and blisters appeared a few days after Taxotere injection

On Day 15 the white cell count turned out to be 1.9 X 10³/μL! That was totally unexpected; the count didn’t increase a bit! Well, the truth is, taxotere’s nadir period is definitely between Day 8 to 14 in my case! Sadly, the doc will have to postpone my next cycle if the blood count did not improve within a week…..

Meanwhile, I have to increase my protein intake and whatever I could get hold of…..

Dairy products and breast cancer – what are the current evidences?

My favourite hot chocolate milk with rum !

I was intrigued by the late Professor Jane Plant’s inspiring story on how she beat cancer by giving up dairy products.  Her story and her books can be found in various websites. When Daily Telegraph published her story in 2014, the article triggered numerous complaints and she was being accused of misleading women by falsely suggesting a link between breast cancer and dairy products. Mind you, we are talking about the multi-million farming business here!

(http://www.telegraph.co.uk/foodanddrink/healthyeating/10868428/Give-up-dairy-products-to-beat-cancer.html).

Well, in my opinion, she was just sharing what she has experienced and how giving up dairy products improved the prognosis of her breast cancer. Similarly, in my case, having to live with benign breast disease with multiple cysts for a couple of years and how a simple dietary change within a short period of time gave me a diagnosis of breast cancer! I guess we missed out something there. 

Deliciously crazy french onion soup with lots of cheese!

A large number of studies have investigated the relation between dairy food consumption and breast cancer risk, unfortunately with conflicting results. Some studies were well-designed but some have obvious flaws. Most cancer-related organizations prefer to take the middle path by saying there were no significant relationship between dairy products intake and cancer.

Nevertheless, there are studies that positively link dairy products intake and risk of cancer worthy of attention!

• In an ecologic study from 1916-1975 where data obtained from the Norwegian Cancer Registry were analysed to compare risk of breast cancer among women who went through the period before, during, or after World War II, breast cancer risk in 1975 was found to be 2.7-times higher than in 1916. This risk has been associated with changes of life style factors after World War II including milk intake (Tretli and Gaard 1996).

• In another prospective study to examine the relationship between energy and fat consumption and the risk of breast cancer among 25,892 Norwegian women, women consuming 0.75 L or more of full-fat milk daily had a relative risk of 2.91 compared with those who consumed 0.15 L or less (Gaard et al. 1995).

• Data from the Nurses' Health Study II found that women who ate red meat and two or more servings of high-fat dairy products (whole milk or butter) every day had a higher risk of breast cancer before menopause (Cho et al. 2003).

• A study and a mean follow up of 11.8 years on 1893 women diagnosed with early-stage invasive breast cancer from 1997 to 2000 concluded that intake of high-fat dairy was related to a higher risk of mortality after breast cancer diagnosis (Kroenke et al. 2013).

• In another recent large Swedish cohort study among people with lactose intolerance, it was demonstrated that people with lactose intolerance and low consumption of milk and other dairy products had a decreased risk of breast, lung, and ovarian cancers (Ji et al. 2015).  

• An increased ovarian cancer risk was observed for whole milk consumption and lactose intake among African-American women in a population-based case-control study (Qin et al. 2016).

• A study to assess differences in dietary intakes in breast cancer survivors and women without a history of breast cancer revealed that survivors tend to consume less dairy products, animal protein, total protein, and calcium, but more legumes, non-citrus fruit, and carbohydrates (Lay et al. 2016).

• Experiments carried out in the laboratory indicated that consumption of commercial whole and non-fat milk for 20 weeks doubled the incidence chemical-induced mammary tumors in rats  (Qin et al. 2007).  

Cheese, glorious cheese......

A variety of mechanisms suggesting ways dairy products influence breast cancer risk was hypothesized.  For example, the presence of components such as calcium, vitamin D, insulin-like growth factors (Ma et al. 2001, Qin et al. 2009), conjugated linoleic acid (Voorrips et al. 2002), and estrogenic hormones (Brinkman et al. 2010) are thought to be contributing to the risks.  

• The Melbourne Collaborative Cohort Study, which included women from Australia, New Zealand, the United Kingdom, Italy, and Greece, found that dairy intake was statistically significantly related to higher levels of estradiol and free estradiol (Brinkman et al. 2010).

• Since estrogens are considered the major etiologic pathway to breast cancer, the influence of dairy intake on estrogens should be strongly considered in understanding how dairy  would affect breast cancer–specific outcome (Kroenke et al. 2013).

Recently, more defined molecular mechanisms were proposed. To appreciate the mechanisms behind milk-induced cell proliferation and growth, we need to understand briefly the role of FTO gene, the microRNAs (miRNAs) found in cow’s milk and the mTORC1 signalling pathways.

• FTO (fat mass- and obesity-associated) gene is widely expressed in a variety of human tissues and is detected in the brain, pancreatic islets, and the liver (Frayling et al. 2007, Bodo C. Melnik 2015). The FTO gene has been recognized to play a crucial role in the early-life determination of body weight, body composition and energy balance (Sebert et al. 2014).

• FTO plays a predominant role in DNA demethylation and m6A-dependent mRNA demethylation (Frayling et al. 2007, Gerken et al. 2007, Jia et al. 2011).  FTO-mediated demethylation of mRNAs increases transcriptional activity and generates mRNA splice variants that are critically involved in adipogenesis  (Zhao et al. 2014), appetite control (Jia et al. 2011), and mTORC1 activation (Gulati et al. 2013, Han et al. 2012). It is important to note that mTORC1 activation eventually leads to cell growth and proliferation and is known to be a marker in breast cancer.

• In addition, FTO promotes transcription and increases genomic transcriptional activity, a requirement for postnatal growth and lactation coordination.   

• FTO also plays a critical role in milk production. The mRNA of prolactin, the most important hormone promoting lactation, is regulated via m6A methylation which was dependent on FTO activity (Bian et al. 2015, Carroll et al. 1990).

Enhancing both milk quality and quantity is a major selection criterion for the genetic improvement of livestock. High performance dairy cows with higher milk yield have an enhanced expression of miRNA-29 (Bian et al. 2015). MiRNAs are non-coding RNA molecules that regulates gene expression.

• Abundance of miRNA-29s increases both bovine FTO mRNA and protein levels of these cells (via inhibition of methylation).  

• DNA methylation is a process which methyl groups are added to DNA, and if the methyl groups are located at the genes, then the genes will not be transcribed or translated into proteins. On the other hand, demethylation is a process that removes the methyl group from the DNA.

• Bovine miRNA-29s, which are identical with human miRNA-29s, and bovine FTO mRNA, which is highly homologous (similar) to human FTO mRNA, are taken up by humans via the uptake of milk exosomes by human macrophages ( a type of immune cell) (Bian et al. 2015).

• In milk, miRNAs are encapsulated in exosomes which are highly resistant against harsh degrading conditions and thus, facilitating uptake by endocytosis. MiRNAs of commercial cow´s milk are known to survive processing such as pasteurization, homogenization and refrigeration (Howard et al. 2015).  

• MiRNAs are known to be absorbed from cow milk and affect gene expression in peripheral blood mononuclear cells of human subjects (Baier et al. 2014). Since, the majority of bovine miRNAs have nucleotide sequences complementary to human gene transcripts; the absorbed miRNAs are likely to regulate human genes (Baier et al. 2014).

   

In short:

• Milk stimulates the expression of FTO, which functions as a critical amplifier of the transcriptional machinery for postnatal growth.

• Milk activates the nutrient-sensitive kinase mechanistic target of rapamycin complex 1 (mTORC1), which induces mTORC1-dependent translation, a crucial requirement for cell growth and proliferation (B. C. Melnik 2015).

• mTORC1 activation eventually leads to increased growth and proliferation and is known to be a marker in certain cancers.

• Milk proteins are a rich nutrient source of branched-chain essential amino acids (BCAAs) and glutamine which also play an important role in FTO expression and mTORC1 activation (Lenders et al. 2009, Millward et al. 2008).  

• In comparison to human breast milk, equivalent volumes of cow´s milk transfer three times more BCAAs to the human and thus may overstimulate BCAA-driven FTO and mTORC1 activation, both of which triggers cell growth (B. C. Melnik 2015).  

In my humble opinion, if you have benign breast diseases, you may want to seriously considering limiting dairy products from your diet. I wished I knew this earlier, but I am definitely not crying over spilled milk!

 

Blissful ice cream......sigh...

References:

Baier SR, Nguyen C, Xie F, Wood JR and Zempleni J (2014). MicroRNAs are absorbed in biologically meaningful amounts from nutritionally relevant doses of cow milk and affect gene expression in peripheral blood mononuclear cells, HEK-293 kidney cell cultures, and mouse livers. J Nutr, 144(10), 1495-1500.

Bian Y, Lei Y, Wang C, Wang J, Wang L, Liu L, et al. (2015). Epigenetic Regulation of miR-29s Affects the Lactation Activity of Dairy Cow Mammary Epithelial Cells. J Cell Physiol, 230(9), 2152-2163.

Brinkman MT, Baglietto L, Krishnan K, English DR, Severi G, Morris HA, et al. (2010). Consumption of animal products, their nutrient components and postmenopausal circulating steroid hormone concentrations. European journal of clinical nutrition, 64(2), 176-183.

Carroll SM, Narayan P and Rottman FM (1990). N6-methyladenosine residues in an intron-specific region of prolactin pre-mRNA. Molecular and cellular biology, 10(9), 4456-4465.

Cho E, Spiegelman D, Hunter DJ, Chen WY, Stampfer MJ, Colditz GA, et al. (2003). Premenopausal fat intake and risk of breast cancer. Journal of the National Cancer Institute, 95(14), 1079-1085.

Frayling TM, Timpson NJ, Weedon MN, Zeggini E, Freathy RM, Lindgren CM, et al. (2007). A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science (New York, N.Y.), 316(5826), 889-894.

Gaard M, Tretli S and Loken EB (1995). Dietary fat and the risk of breast cancer: a prospective study of 25,892 Norwegian women. Int J Cancer, 63(1), 13-17.

Gerken T, Girard CA, Tung YC, Webby CJ, Saudek V, Hewitson KS, et al. (2007). The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylase. Science (New York, N.Y.), 318(5855), 1469-1472.

Gulati P, Cheung MK, Antrobus R, Church CD, Harding HP, Tung YC, et al. (2013). Role for the obesity-related FTO gene in the cellular sensing of amino acids. Proceedings of the National Academy of Sciences of the United States of America, 110(7), 2557-2562.

Han JM, Jeong SJ, Park MC, Kim G, Kwon NH, Kim HK, et al. (2012). Leucyl-tRNA synthetase is an intracellular leucine sensor for the mTORC1-signaling pathway. Cell, 149(2), 410-424.

Howard KM, Jati Kusuma R, Baier SR, Friemel T, Markham L, Vanamala J, et al. (2015). Loss of miRNAs during processing and storage of cow's (Bos taurus) milk. Journal of agricultural and food chemistry, 63(2), 588-592.

Ji J, Sundquist J and Sundquist K (2015). Lactose intolerance and risk of lung, breast and ovarian cancers: aetiological clues from a population-based study in Sweden. British journal of cancer, 112(1), 149-152.

Jia G, Fu Y, Zhao X, Dai Q, Zheng G, Yang Y, et al. (2011). N6-methyladenosine in nuclear RNA is a major substrate of the obesity-associated FTO. Nature chemical biology, 7(12), 885-887.

Kroenke CH, Kwan ML, Sweeney C, Castillo A and Caan BJ (2013). High- and Low-Fat Dairy Intake, Recurrence, and Mortality After Breast Cancer Diagnosis. Journal of the National Cancer Institute, 105(9), 616-623.

Lay WA, Vickery CR, Ward-Ritacco CL, Johnson KB, Berg AC, Evans EM, et al. (2016). Comparison of Intake of Animal and Plant Foods and Related Nutrients in Postmenopausal Breast Cancer Survivors and Controls. Journal of nutrition in gerontology and geriatrics, 35(1), 15-31.

Lenders CM, Liu S, Wilmore DW, Sampson L, Dougherty LW, Spiegelman D, et al. (2009). Evaluation of a novel food composition database that includes glutamine and other amino acids derived from gene sequencing data. European journal of clinical nutrition, 63(12), 1433-1439.

Ma J, Giovannucci E, Pollak M, Chan JM, Gaziano JM, Willett W, et al. (2001). Milk intake, circulating levels of insulin-like growth factor-I, and risk of colorectal cancer in men. Journal of the National Cancer Institute, 93(17), 1330-1336.

Melnik BC (2015). Milk--A Nutrient System of Mammalian Evolution Promoting mTORC1-Dependent Translation. International journal of molecular sciences, 16(8), 17048-17087.

Melnik BC (2015). Milk: an epigenetic amplifier of FTO-mediated transcription? Implications for Western diseases. Journal of Translational Medicine, 13, 385.

Millward DJ, Layman DK, Tome D and Schaafsma G (2008). Protein quality assessment: impact of expanding understanding of protein and amino acid needs for optimal health. Am J Clin Nutr, 87(5), 1576s-1581s.

Qin B, Moorman PG, Alberg AJ, Barnholtz-Sloan JS, Bondy M, Cote ML, et al. (2016). Dairy, calcium, vitamin D and ovarian cancer risk in African-American women. British journal of cancer, 115(9), 1122-1130.

Qin LQ, He K and Xu JY (2009). Milk consumption and circulating insulin-like growth factor-I level: a systematic literature review. International journal of food sciences and nutrition, 60 Suppl 7, 330-340.

Qin LQ, Xu JY, Tezuka H, Li J, Arita J, Hoshi K, et al. (2007). Consumption of commercial whole and non-fat milk increases the incidence of 7,12-dimethylbenz(a)anthracene-induced mammary tumors in rats. Cancer detection and prevention, 31(4), 339-343.

Sebert S, Salonurmi T, Keinanen-Kiukaanniemi S, Savolainen M, Herzig KH, Symonds ME, et al. (2014). Programming effects of FTO in the development of obesity. Acta physiologica (Oxford, England), 210(1), 58-69.

Tretli S and Gaard M (1996). Lifestyle changes during adolescence and risk of breast cancer: an ecologic study of the effect of World War II in Norway. Cancer causes & control : CCC, 7(5), 507-512.

Voorrips LE, Brants HA, Kardinaal AF, Hiddink GJ, van den Brandt PA and Goldbohm RA (2002). Intake of conjugated linoleic acid, fat, and other fatty acids in relation to postmenopausal breast cancer: the Netherlands Cohort Study on Diet and Cancer. Am J Clin Nutr, 76(4), 873-882.

Zhao X, Yang Y, Sun BF, Shi Y, Yang X, Xiao W, et al. (2014). FTO-dependent demethylation of N6-methyladenosine regulates mRNA splicing and is required for adipogenesis. Cell research, 24(12), 1403-1419.

A brief review on Opuntia megacantha (Opuntia ficus-indica (L.) Mill ), a major component of the Millennium® Powdered Beverage (E. Excel International)

[source of picture : http://www.thelovelyplants.com/striking-landscape-plant-opuntia-ficus-indica-prickly-pear/]

The first gift I received from my family upon my diagnosis was the Millennium® Powdered Beverage. The exclusive gold coloured packaging clearly reflected its price! I nearly choked up and was in tears when I found out that it cost a few hundred bucks for the price of 30 sachets!

My sister proudly said “This will help boost up your immune system and strength, drink 1 or 2 sachets a day to keep yourself strong to fight!” Well, I was smart not to get myself in trouble by asking too many questions (ehem…proven evidences etc). I have read about Nutritional Immunology and thus, I totally agree with the concept of nutrition and immune system. Ehem...since this product is so expensive and a best-selling item, I should be expecting some results there…..

The main ingredient in the Millenium series of products eg. Millennium® and Millennium® Red is the Millennium® Cactus Blend comprising prickly pear cactus pad extract and other ingredients. On the other hand, the Millennium® Powdered Beverage is a proprietary blend consisting of cactus powder, cactus, orange powder, lemon powder, fructose, maltodextrin and stevia. Unfortunately, I could not find any information to confirm that the “cactus components” mentioned are derived from the prickly pear cactus pad extract or any specific part of the cactus plant.  

Anyway the cactus species used in these products is Opuntia megacantha Salm-Dyck. It is also known as Opuntia ficus-indica (L.) Mill (http://www.theplantlist.org/tpl1.1/record/kew-2391644) and belongs to the dicotyledonous angiosperm Cactaceae family, a family with at least 1500 species of cactus.  Common names include prickly pear or nopal cactus.

O. ficus-indica is grown for the large, sweet fruits (often called “tunas”) in regions such as Mexico, Sicily, Algeria, Chile, Brazil, and northern Africa (Griffith 2004). The young cladodes (stem segments) of O. ficus-indica are usually harvested as a vegetable crop. Apparently, the medicinal properties of this cactus species have been documented as early as 1552! (Griffith 2004).  

Prickly pear cactus is used in the forms of tea, jam, juice and oil extracted from prickly pear seeds, for health, nutrition or cosmetic purposes. Opuntia species have been used for thousands of years as a folk medicine and as a herbal remedy for a diverse of health problems in various countries (El-Mostafa et al. 2014). Traditionally, it is used to treat ulcers, diarrhoea, burns, wounds, edema, hyperlipidemia, obesity, aging, gastritis and inflammation.

A search in Pubmed with the keyword “Opuntia ficus-indica” yielded more than 250 studies, clearly indicating that this plant is well-researched. A number of in vitro and in vivo (animal) studies were carried out to provide substantial evidences supporting its diverse pharmacological activities. Only a few clinical trials were conducted in areas such as obesity and weight loss. Interestingly, a clinical trial among healthy subjects concluded that consumption of cactus pear fruit positively affects the body's redox balance, decreases oxidative damage to lipids, and improves antioxidant status in healthy humans (Tesoriere et al. 2004).  Unfortunately, there weren’t any clinical evidences supporting the claim that cactus extracts improve the human immune status or function!

Cactus fruit contains substantial amounts of ascorbic acid, vitamin E, carotenoids, fibers, amino acids and antioxidant compounds (phenols, flavonoids, betaxanthin and betacyanin). Several reports have also mentioned the abundance of vitamins and minerals such as calcium and potassium (Ammar et al. 2015, Mata et al. 2016, Stintzing et al. 2001, Stintzing et al. 2003).

In addition, some of the main constituents identified and present in the extract are flavonoids, namely isorhamnetins and derivatives such as isorhamnetin 3-O-rhamnose-rutinoside and isorhamnetin 3-O-rutinoside) and phenolic acids (such as ferulic, piscidic and eucomic acids). These compounds and flavanoid-rich extracts are known to function effectively as antioxidants and anti-inflammatory components (Antunes-Ricardo et al. 2015, Chaouch et al. 2015, Kim et al. 2015, Matias et al. 2014, Nakahara et al. 2015, Yeddes et al. 2014). Other flavonoids such as quercetin, (+)-dihydroquercetin, and quercetin 3-methyl ether are also found in the fruits and stems of O. ficus-indica and are reported to have neuroprotective actions against the oxidative injuries in brain cells (Dok-Go et al. 2003).

Large quantities of GABA (γ-Aminobutyric acid) have been detected in the cactus extract. Proline (Pro) and Glutamine (Gln) are the most abundant amino acids in prickly pear fruits.  Ornithine, Citrulline and 2-aminoethanolamine have also been detected in low amounts in the juices (Ali et al. 2014, Kugler et al. 2006). Interestingly, and from a nutritional aspect, the relatively large quantities of Gln, and Pro are of interest as these amino acids are considered as functional amino acids, or key metabolic amino acids (Wu 2010). We all know that foods containing GABA is beneficial for mental health, as GABA is a key neurotransmitter in the brain for stress relief and relaxation. Well, one needs GABA to feel calm, relaxed and happy!

Cactus pear extracts effectively inhibited cell growth in several different immortalized and cancer cell cultures, suppressed tumor growth in nude mice, and modulated expression of tumor-related genes, thus emphasizing the chemoprevention and anti-tumor properties of this plant (Keller et al. 2015, Zou et al. 2005).  Unfortunately there was no laboratory or animal data on how the cactus extracts improves or strengthens the immune cells or system!

My personal experience with this product

The powdered extract when mixed with a glass of water gives a mild lemony flavoured drink. Not sweet but pleasant and soothing to the queasy stomach (especially after chemotherapy). I took it at least once daily after my surgery and throughout the FEC chemotherapy sessions. Luckily, I neither needed any immune booster jab (filgrastim) nor was I down with illness such as sore throat, flu, cough or mouth ulcers. I am not sure if this product helped, as I also took a lot of coconut water, beetroot juice, napier grass and barley drink! I would say that I am eating well and adequately nourished! Could all these be contributing factors? I am not sure…..but cactus extracts are pretty darn expensive!

I increase the dose to twice daily after my 5^th cycle Taxotere injection. I developed a bad allergy towards filgrastim (immune booster jab) during my 4^th cycle, and thus I have to skip this drug for good. Fortunately, so far, my blood work was ok without filgrastim! 

In conclusion, I think cactus pear extract is an excellent source of antioxidants, anti-inflammatory components, vitamins, minerals and functional acid amino. It fits the description of an impressive functional food and should be beneficial for patients in different stages of recovery. Generally, patients who are eating well and adequately nourished with balance nutrition are usually the ones able to cope and manage the harsh side effects of chemotherapy.

References:

Ali HSM, Al-Khalifa AS and Brückner H (2014). Taurine is absent from amino components in fruits of Opuntia ficus-indica. SpringerPlus, 3, 663.

Ammar I, Ennouri M, Bouaziz M, Ben Amira A and Attia H (2015). Phenolic Profiles, Phytchemicals and Mineral Content of Decoction and Infusion of Opuntia ficus-indica Flowers. Plant Foods Hum Nutr, 70(4), 388-394.

Antunes-Ricardo M, Gutierrez-Uribe JA, Martinez-Vitela C and Serna-Saldivar SO (2015). Topical anti-inflammatory effects of isorhamnetin glycosides isolated from Opuntia ficus-indica. BioMed research international, 2015, 847320.

Chaouch MA, Hafsa J, Rihouey C, Le Cerf D and Majdoub H (2015). Depolymerization of polysaccharides from Opuntia ficus indica: Antioxidant and antiglycated activities. International journal of biological macromolecules, 79, 779-786.

Dok-Go H, Lee KH, Kim HJ, Lee EH, Lee J, Song YS, et al. (2003). Neuroprotective effects of antioxidative flavonoids, quercetin, (+)-dihydroquercetin and quercetin 3-methyl ether, isolated from Opuntia ficus-indica var. saboten. Brain Research, 965(1–2), 130-136.

El-Mostafa K, El Kharrassi Y, Badreddine A, Andreoletti P, Vamecq J, El Kebbaj M, et al. (2014). Nopal Cactus (Opuntia ficus-indica) as a Source of Bioactive Compounds for Nutrition, Health and Disease. Molecules, 19(9), 14879.

Griffith MP (2004). The origins of an important cactus crop, Opuntia ficus-indica (Cactaceae): new molecular evidence. American Journal of Botany, 91(11), 1915-1921.

Keller J, Camare C, Bernis C, Astello-Garcia M, de la Rosa AP, Rossignol M, et al. (2015). Antiatherogenic and antitumoral properties of Opuntia cladodes: inhibition of low density lipoprotein oxidation by vascular cells, and protection against the cytotoxicity of lipid oxidation product 4-hydroxynonenal in a colorectal cancer cellular model. Journal of physiology and biochemistry, 71(3), 577-587.

Kim J, Soh SY, Shin J, Cho CW, Choi YH and Nam SY (2015). Bioactives in cactus (Opuntia ficus-indica) stems possess potent antioxidant and pro-apoptotic activities through COX-2 involvement. Journal of the science of food and agriculture, 95(13), 2601-2606.

Kugler F, Graneis S, Schreiter PP, Stintzing FC and Carle R (2006). Determination of free amino compounds in betalainic fruits and vegetables by gas chromatography with flame ionization and mass spectrometric detection. Journal of agricultural and food chemistry, 54(12), 4311-4318.

Mata A, Ferreira JP, Semedo C, Serra T, Duarte CM and Bronze MR (2016). Contribution to the characterization of Opuntia spp. juices by LC-DAD-ESI-MS/MS. Food chemistry, 210, 558-565.

Matias A, Nunes Sl Fau - Poejo J, Poejo J Fau - Mecha E, Mecha E Fau - Serra AT, Serra At Fau - Madeira PJA, Madeira Pj Fau - Bronze MR, et al. (2014). Antioxidant and anti-inflammatory activity of a flavonoid-rich concentrate recovered from Opuntia ficus-indica juice. (2042-650X (Electronic)).

Nakahara T, Mitoma C, Hashimoto-Hachiya A, Takahara M, Tsuji G, Uchi H, et al. (2015). Antioxidant Opuntia ficus-indica Extract Activates AHR-NRF2 Signaling and Upregulates Filaggrin and Loricrin Expression in Human Keratinocytes. Journal of medicinal food, 18(10), 1143-1149.

Stintzing FC, Schieber A and Carle R (2001). Phytochemical and nutritional significance of cactus pear. European Food Research and Technology, 212(4), 396-407.

Stintzing FC, Schieber A and Carle R (2003). Evaluation of colour properties and chemical quality parameters of cactus juices. European Food Research and Technology, 216(4), 303-311.

Tesoriere L, Butera D, Pintaudi M, Allegra M and Livrea MA (2004). Supplementation with cactus pear (Opuntia ficus-indica) fruit decreases oxidative stress in healthy humans: a comparative study with Vit C. Am J Clin Nutr, 80.

Wu G (2010). Functional amino acids in growth, reproduction, and health. Advances in nutrition (Bethesda, Md.), 1(1), 31-37.

Yeddes N, Cherif JK and Trabelsi Ayadi M (2014). Comparative study of antioxidant power, polyphenols, flavonoids and betacyanins of peel and pulp of three Tunisian Opuntia forms. Pakistan journal of biological sciences : PJBS, 17(5), 650-658.

Zou D-m, Brewer M, Garcia F, Feugang JM, Wang J, Zang R, et al. (2005). Cactus pear: a natural product in cancer chemoprevention. Nutrition Journal, 4(1), 25.