The Breast Feeding Ballet: Nurse, Supplement, Pump, Repeat

breast pumping

It’s 4:36 a.m. As I sit here at my computer typing this post, the sound of my breast pump hisses in the background.

I’ve been up most of the night nursing my baby girl and trying to soothe her back to sleep. When I finish, I pump for a few minutes in an effort to increase my milk supply and preserve every precious last drop. Then I drift off to sleep for an hour or so before it’s time to start the whole process again.

It’s times like these that I often wish I was bottle-feeding.

Don’t get me wrong — I love breast-feeding, but sometimes it can be exhausting. I breast-fed my son, James, for 14 months, stopping only when I got pregnant with Diana and my supply significantly decreased. I don’t think I would have continued much longer anyway. I was ready to wean him at that point — I was getting sick of pumping and the never-ending cycle of washing pump parts. I also did not want to be breast-feeding a child that could ask for it by name, and we were closely approaching that territory at 14 months. By the way if you want to buy breast pump you can try these best quality breast pump.

But it was bittersweet when I finally stopped. I missed those sweet, tender moments we shared when I would look down at him snuggled against my breast, nursing contently. It’s a bond only a mother and child can share, and it is an amazing feeling.

Before I had both my kids, I would often get asked whether I was going to breast-feed. My approach both times was similar to my birth plan — to go with the flow. I wanted to try to breast-feed, but if it didn’t work out, I said I wouldn’t beat myself up over it and we would switch to formula.

I had heard from many friends how difficult breast-feeding could be. People told me horror stories about the pain. Others told me that they tried it, it didn’t go well, neither mom nor baby was happy, so they gave up and switched to formula and everyone was much happier. Others told me that they didn’t even try because they just didn’t want to.

I was relieved to hear my friends’ experiences. It made me feel like there were options. It also helped knowing that not everyone was successful. I was afraid of getting frustrated and feeling like a failure if I could not do it. So when I was asked whether I was going to breast-feed, I would just say, “I am going to try,” and leave it at that.

Before James was born, I took a breast-feeding class and read books on breast-feeding. They both made me feel overwhelmed and confused. I don’t think it’s something that you can really prepare for or practice until you actually try.

The one thing I did that I think helped tremendously was ask for help. James didn’t latch on right away after he was born. I panicked because I’d heard that immediately after birth is the best time to breast-feed, and if you don’t get it then, the baby might never latch on.

I can tell you that just isn’t true. I tried and tried to get him to latch on, but he just wouldn’t. I wasn’t sure if it was because of his cleft lip, or if it was error on my part. So I started asking for help from anyone who was willing to help me — nurses, lactation consultations, etc. I threw all modesty out the window and quickly got comfortable with people I didn’t know seeing and even touching my breasts and watching me breast-feed. I did the same thing with Diana: I took advantage of the lactation consultants in the hospital and asked for help immediately to make sure we were getting it right. It definitely came easier with the second baby.

Still, my experience has not been problem-free. When I had James, I had to be on blood pressure medication for six weeks after delivery. The medication decreased my milk supply, and James was clearly not getting enough during feedings, so we had to supplement with formula after every feeding. I’m on a similar blood pressure medication now after developing pre-eclampsia with this pregnancy, which has also led to a decrease in my supply.

Also, Diana isn’t back to her birth weight or gaining weight as quickly as we’d like, so we’re in a pattern of nurse, supplement, pump, repeat. I’m also taking Fenugreek herbal supplements, drinking Mother’s Milk tea and a beer a day (which I’ve heard may or may not help increase milk production). I’m not sure that any of these things are really helping, but I’m willing to try anything, and I’m definitely enjoying my daily beer!

It’s time-consuming trying to increase my milk supply, but the only part that really bothers me is pumping. I don’t know what it is, but I really don’t enjoy being hooked up to that machine. It seems to interrupt the natural flow of things. Right after I feed Diana, I want to hold her and snuggle with her when she is full and at her happiest. Instead, I have to either pass her off to someone or put her down while I hook myself up to the pump. Then I have to clean all those parts. Ugghh. It takes forever.

My dislike of pumping only grew when I went back to work after I had James. I am lucky enough to have an office with a lock, so I could pump right in my office. Still, it was inevitable that someone would knock on the door as soon as I sat down to pump. In an office full of men, it’s embarrassing to yell through the door, “Come back in 10 minutes. I’m pumping.” The first time I had to travel for work, I ended up with a nasty case of mastitis (an infection in the tissue of the breast). Then there was the time I forgot my pump at home. I tried to express some milk by hand to relieve the pressure, but by early afternoon I was so uncomfortable I had to go home. I made sure to never do that again.

When I’m at home, I breast-feed or pump in front of anyone who’s around. I try to be discreet about it, and I can situate my shirt in a way not to reveal too much, but I know some people have seen more than they might have liked. I have a cover-up, but it’s too much of a hassle for me to get it out. Besides, it’s my house and if someone isn’t comfortable with it, they can leave.

I feel comfortable enough to breast-feed in public, but I find that if I do, I get disapproving looks of disgust from many people, even if I am wearing a cover-up. So if I go out in public and have to nurse, I tend to go to a women’s rest room with a couch, or even sit in the back seat of my car. It’s not the most convenient, but it makes me more comfortable than getting the evil eye. That’s the thing I don’t get: Everyone seems to say breast-feeding is best for the baby, and everyone wants mothers to do it, but no one actually wants to make it easy for us to do it. We shouldn’t be made to feel that it’s dirty or shameful. We are just trying to feed and nurture our babies.

With James, my supply increased and we went on to have a very successful breast-feeding relationship once I was able to wean off the blood pressure medication. I’m hoping the same thing will happen with Diana, but if it doesn’t, and I have to stop breast-feeding, I know it’s not the end of the world. I know plenty of kids who weren’t breast-fed, and they all turned out just fine.

And it’s not that I have any problems or issues with formula or bottle-feeding. It’s solely selfishness on my part that I just want to breast-feed. I feel down on myself because my baby can’t get all that she needs from me. It’s frustrating when I feed her and I can tell she is just not satisfied. Maybe it’s my Italian side that’s always concerned with food, but it stresses me out when I know my baby is still hungry, and not content or full.

I love that milk coma that she slips into when she has a successful feeding or takes extra milk from the bottle. That makes me happy, and I feel like I’m doing my job. I can’t wait until we go to the doctor and she’s gotten back to her birth weight. Maybe then I’ll be able to relax and not worry about her feedings so much.

Medical Nutrition Management in Parkinson’s Disease

Parkinson’s Disease

Parkinson’s disease is an irreversible neurological disorder resulting from lowered levels of the neurotransmitter, dopamine, at the basal ganglia of the brain and typically results in trembling, rigidity, slowness of gain, insomnia, incoordination, constipation, cognitive decline and other systemic symptoms. Approximately 1.5 million people in the US have Parkinson’s syndrome. There is no cure, only symptomatic relief of which L-Dopa, the precursor to dopamine and product of tyrosine metabolism, is administered along with other supportive medications such as anti-depressants or MAO Inhibitors.

Although there is a strong genetic component to Parkinson’s Disease (PD), only about 10% are truly genetic. The remainder of the cases are thought to be results of long-term exposure to manganese, lead, iron, pesticides, herbicides, contaminated well water or even medications such as major tranquilizers and benzodiazepines. Other predisposing factors are head trauma/injury, high intake of red meat and heme iron, low caffeine intakes (in women, but not men), & vitamin D deficiency (but not directly). Genetic aberrations in how iron is handled have been found with alterations in transferrin and the hemochromatosis gene meaning that iron metabolism is deregulated which may account for the iron deposits found in the brains of PD patients.

Neuroprotection is being studied as a means of protecting the nervous system and brain from the ravages of PD as L-Dopa, the primary treatment of choice, grows less effective as time wears on. Nutritionists are looking at dietary factors that can prevent oxidation, provide neuroprotection and offer supportive functions where the metabolic pathways have become ineffectual. (1)

The Role of Macronutrients Macronutrients refers to proteins, fats, carbohydrates and fibers in the diet. The amounts, types and distribution of each of these nutrients play a key supportive and therapeutic role in the nutritional treatment of PD. If an overall diet plan were to be chosen, the Mediterranean Diet eating plan would be the template for any dietary modifications since it is consistently favored in the literature as a preventative dietary approach for PD.

Protein

L-Dopa, the major therapeutic treatment for PD, competes with the amino acids from protein fragments for absorption. Consequently, low protein diets, either .5g/kg or a straight 40 g protein diet, are therapeutically recommended to enhance the effectiveness of L-Dopa absorption at its lowest possible dose for the longest period of time possible. The protein limit prior to the last meal of the day is 7 grams according to one study (2). Generally, protein loads are advised for the evening meal with mostly carbohydrates, fiber, fats and fluids throughout the day. This means the daily diet should consist of fruits, vegetables, some grains, water, juice, limited nuts and nut butter and low protein medical foods. While dairy is important, do not take it with medications or within 40 minutes after L-Dopa as it, too, contains proteins.

Fats Fats are classified as either saturated, polyunsaturated or monounsaturated. Early studies in rats showed a detrimental effect of total fat on PD progression. Later studies in humans showed more of a negative relationship to animal fats in PD progression. Saturated fat theoretically alters the cell membrane adversely affecting the lipid membrane and promoting oxidative stress. (2)

Neuroprotection has been found with diets high in polyunsaturated fats(PUFA), particularly with the omega-3 fatty acids. It has also been consistently shown that diets high in PUFA and low in saturated fats reduce the risk of PD and protect from the toxic effects of neurotoxins.

Saturated fats, found abundantly in meats, are loaded with the “heme” protein, a protein some PD patients are genetically programmed not to metabolize correctly, thus aggravating symptoms and possibly accounting for the negative associations between meat consumption and PD development. (2)

Carbohydrates

Carbohydrates may play a more positive role in decreasing progression of PD. Carbohydrates are full of polyphenols, fibers and increase the release of insulin-induced dopamine in the brain. Since a high consumption of carbohydrates is not necessarily beneficial for everyone, particularly those with diabetes, emphasis should be placed on fiber containing carbohydrates rather than simple sugars.

Fiber Constipation is a common complaint in patients with PD as is adequate fluid intake. Getting enough fiber will help to avoid constipation and straining, but an increase should be gradual to avoid gas and bloating and should be accompanied by an intake of 8-10 glasses of fluids per day. Twenty-five grams of fiber a day is the current daily recommendation.

The Role of Micronutrients

Supportive Supplements

Some nutrients have been identified to have a supportive role in PD preventing oxidation and neurodegeneration thus delaying or mitigating symptoms associated with the demise associated with this disorder.

Omega 3 Fatty Acids Omega 3’s have proven to be a protective factor in many neurodegenerative diseases. (2) Oral administration of docosahexaenoic acid (DHA), an omega 3 fatty acid, increases dopaminergic neurotransmission, synaptic membrane formation as well as the density of dendrite spines. In the first study of its kind, DHA supplementation in rats was shown to have neurorestorative and disease-modifying properties. (3) Supplements of 1,000 mg of DHA/EPA omega 3 fatty acids may be supportive in the prevention of the ravages of PD.

Of all supplements studied, only fish oil (a source of omega 3’s and coenzyme Q10 showed significant associations with PD progression. (4)

B-Vitamins

Both folic acid and B12 have commonly been supplemented in PD. Both are known to lower the neurotoxin homocysteine and are often low in PD patients. Patients on L-Dopa must frequently limit their B6 intake to 15 mg so as to not interfere with L-Dopa.

Coenzyme Q10

Coenzyme Q10 is a naturally occurring, fat-soluble, vitamin-like enzyme found in a variety of foods and synthesized in the body. At levels of 300,600 and 1200 mg/day over a six-month period, patients showed decreasing symptoms over placebo with the best effects achieved at the 1200 mg supplementation level.(5,6)

Vitamin D All patients with PD should have their vitamin D checked and repleted if low. Much debate exists over the optimum blood level of this pro-hormone, but its importance in multiple system disease management can no longer be questioned. Since the intake of milk and vitamin D fortified products is often low in PD patients, supplementation is often needed and required for optimum prevention of future neurological demise. Repletion therapy involves high doses of 10,000 IU/day for 5 days per week for six weeks and then retest. Maintenance dose can be anywhere from 400 – 1000 IU/day after repletion therapy.

The Role of Nutraceuticals

Green Tea

While black tea is a no-no due to its high manganese level, green tea has shown beneficial effects at about 3 cups per day. Green tea has both anti-oxidant and anti-inflammatory properties and has been shown to have neuroprotective qualities (7). It is thought that the polyphenols and, specifically, epigallocatechin gallate (EGCG), a catechin, are responsible for the beneficial effects.

Melatonin

Melatonin is a hormone synthesized by several tissues other than the pineal gland in the brain that exerts neuroprotective, anti-inflammatory, antioxidant and regulatory effects on the body. Melatonin has been shown to improve motor derangement, non—motor symptoms, sleep and anxiety disorders as well as improving memory and decreasing depression in PD patients. Current research suggests its use in preventing the neurodegeneration in PD. (8) Melatonin is also known to decrease homocysteine, a chemical that is neurotoxic to dopaminergic neurons in PD patients and is a known cardiovascular risk indicator (9).

Because, theoretically, melatonin can cause a decrease in dopamine secretion, it is suggested that therapy begin low and slow at 1 mg in the evening before bed and increasing up to 5 mg if tolerated.

Additional Supportive Practices In cases of heavy metal poisoning, eating foods high in sulfur may assist the detoxification process. Foods such as onions, garlic, and foods high in water soluble fibers from guar gum, pectin, oats, oat bran and psyllium seeds. Maintaining a high antioxidant intake of vitamin C and bioflavonoids from vegetables and fruits are helpful as well as lowering meat intake.

In the initial stages of PD, caloric restriction of up to 25% of estimated needs may help alleviate some symptoms, but over time weight loss and adequate caloric intake become of paramount importance to prevent malnutrition. Hydration and choking may become issues of concern. Food may then need to be blenderized and ways to increase calories may need to be implemented to prevent excess weight loss. A weight loss of greater than 10% in six months is high risk for malnutrition and should be addressed by a Dietitian.

Parkinson’s disease is an irreversible neurological disorder resulting from lowered levels of the neurotransmitter, dopamine, at the basal ganglia of the brain and typically results in trembling, rigidity, slowness of gain, insomnia, incoordination, constipation, cognitive decline and other systemic symptoms. Approximately 1.5 million people in the US have Parkinson’s syndrome. There is no cure, only symptomatic relief of which L-Dopa, the precursor to dopamine and product of tyrosine metabolism, is administered along with other supportive medications such as anti-depressants or MAO Inhibitors.

Although there is a strong genetic component to Parkinson’s Disease (PD), only about 10% are truly genetic. The remainder of the cases are thought to be results of long-term exposure to manganese, lead, iron, pesticides, herbicides, contaminated well water or even medications such as major tranquilizers and benzodiazepines. Other predisposing factors are head trauma/injury, high intake of red meat and heme iron, low caffeine intakes (in women, but not men), & vitamin D deficiency (but not directly). Genetic aberrations in how iron is handled have been found with alterations in transferrin and the hemochromatosis gene meaning that iron metabolism is deregulated which may account for the iron deposits found in the brains of PD patients. Neuroprotection is being studied as a means of protecting the nervous system and brain from the ravages of PD as L-Dopa, the primary treatment of choice, grows less effective as time wears on. Nutritionists are looking at dietary factors that can prevent oxidation, provide neuroprotection and offer supportive functions where the metabolic pathways have become ineffectual. (1)

The Role of Macronutrients ​ Macronutrients refers to proteins, fats, carbohydrates and fibers in the diet. The amounts, types and distribution of each of these nutrients play a key supportive and therapeutic role in the nutritional treatment of PD. If an overall diet plan were to be chosen, the Mediterranean Diet eating plan would be the template for any dietary modifications since it is consistently favored in the literature as a preventative dietary approach for PD. Protein L-Dopa, the major therapeutic treatment for PD, competes with the amino acids from protein fragments for absorption. Consequently, low protein diets, either .5g/kg or a straight 40 g protein diet, are therapeutically recommended to enhance the effectiveness of L-Dopa absorption at its lowest possible dose for the longest period of time possible. The protein limit prior to the last meal of the day is 7 grams according to one study (2). Generally, protein loads are advised for the evening meal with mostly carbohydrates, fiber, fats and fluids throughout the day. This means the daily diet should consist of fruits, vegetables, some grains, water, juice, limited nuts and nut butter and low protein medical foods. While dairy is important, do not take it with medications or within 40 minutes after L-Dopa as it, too, contains proteins.

Fats Fats are classified as either saturated, polyunsaturated or monounsaturated. Early studies in rats showed a detrimental effect of total fat on PD progression. Later studies in humans showed more of a negative relationship to animal fats in PD progression. Saturated fat theoretically alters the cell membrane adversely affecting the lipid membrane and promoting oxidative stress. (2)

Neuroprotection has been found with diets high in polyunsaturated fats(PUFA), particularly with the omega-3 fatty acids. It has also been consistently shown that diets high in PUFA and low in saturated fats reduce the risk of PD and protect from the toxic effects of neurotoxins.

Saturated fats, found abundantly in meats, are loaded with the “heme” protein, a protein some PD patients are genetically programmed not to metabolize correctly, thus aggravating symptoms and possibly accounting for the negative associations between meat consumption and PD development. (2)

Carbohydrates

Carbohydrates may play a more positive role in decreasing progression of PD. Carbohydrates are full of polyphenols, fibers and increase the release of insulin-induced dopamine in the brain. Since a high consumption of carbohydrates is not necessarily beneficial for everyone, particularly those with diabetes, emphasis should be placed on fiber containing carbohydrates rather than simple sugars. Fiber Constipation is a common complaint in patients with PD as is adequate fluid intake. Getting enough fiber will help to avoid constipation and straining, but an increase should be gradual to avoid gas and bloating and should be accompanied by an intake of 8-10 glasses of fluids per day. Twenty-five grams of fiber a day is the current daily recommendation.

The Role of Micronutrients

Supportive Supplements

Some nutrients have been identified to have a supportive role in PD preventing oxidation and neurodegeneration thus delaying or mitigating symptoms associated with the demise associated with this disorder.

Omega 3 Fatty Acids Omega 3’s have proven to be a protective factor in many neurodegenerative diseases. (2) Oral administration of docosahexaenoic acid (DHA), an omega 3 fatty acid, increases dopaminergic neurotransmission, synaptic membrane formation as well as the density of dendrite spines. In the first study of its kind, DHA supplementation in rats was shown to have neurorestorative and disease-modifying properties. (3) Supplements of 1,000 mg of DHA/EPA omega 3 fatty acids may be supportive in the prevention of the ravages of PD.

Of all supplements studied, only fish oil (a source of omega 3’s and coenzyme Q10 showed significant associations with PD progression. (4)

B-Vitamins Both folic acid and B12 have commonly been supplemented in PD. Both are known to lower the neurotoxin homocysteine and are often low in PD patients. Patients on L-Dopa must frequently limit their B6 intake to 15 mg so as to not interfere with L-Dopa.

Coenzyme Q10 Coenzyme Q10 is a naturally occurring, fat-soluble, vitamin-like enzyme found in a variety of foods and synthesized in the body. At levels of 300,600 and 1200 mg/day over a six-month period, patients showed decreasing symptoms over placebo with the best effects achieved at the 1200 mg supplementation level.(5,6)Vitamin D All patients with PD should have their vitamin D checked and repleted if low. Much debate exists over the optimum blood level of this pro-hormone, but its importance in multiple system disease management can no longer be questioned. Since the intake of milk and vitamin D fortified products is often low in PD patients, supplementation is often needed and required for optimum prevention of future neurological demise. Repletion therapy involves high doses of 10,000 IU/day for 5 days per week for six weeks and then retest. Maintenance dose can be anywhere from 400 – 1000 IU/day after repletion therapy. The Role of Nutraceuticals Green Tea While black tea is a no-no due to its high manganese level, green tea has shown beneficial effects at about 3 cups per day. Green tea has both anti-oxidant and anti-inflammatory properties and has been shown to have neuroprotective qualities (7). It is thought that the polyphenols and, specifically, epigallocatechin gallate (EGCG), a catechin, are responsible for the beneficial effects.

Melatonin Melatonin is a hormone synthesized by several tissues other than the pineal gland in the brain that exerts neuroprotective, anti-inflammatory, antioxidant and regulatory effects on the body. Melatonin has been shown to improve motor derangement, non—motor symptoms, sleep and anxiety disorders as well as improving memory and decreasing depression in PD patients. Current research suggests its use in preventing the neurodegeneration in PD. (8) Melatonin is also known to decrease homocysteine, a chemical that is neurotoxic to dopaminergic neurons in PD patients and is a known cardiovascular risk indicator (9). Because, theoretically, melatonin can cause a decrease in dopamine secretion, it is suggested that therapy begin low and slow at 1 mg in the evening before bed and increasing up to 5 mg if tolerated.

Additional Supportive Practices In cases of heavy metal poisoning, eating foods high in sulfur may assist the detoxification process. Foods such as onions, garlic, and foods high in water soluble fibers from guar gum, pectin, oats, oat bran and psyllium seeds. Maintaining a high antioxidant intake of vitamin C and bioflavonoids from vegetables and fruits are helpful as well as lowering meat intake.

In the initial stages of PD, caloric restriction of up to 25% of estimated needs may help alleviate some symptoms, but over time weight loss and adequate caloric intake become of paramount importance to prevent malnutrition. Hydration and choking may become issues of concern. Food may then need to be blenderized and ways to increase calories may need to be implemented to prevent excess weight loss. A weight loss of greater than 10% in six months is high risk for malnutrition and should be addressed by a Dietitian.

Multivitamins with added iron or manganese should be avoided. Caffeine is acceptable and may provide some benefit to brain and energy function. Kava kavva, Ephedra, Ma Huang, Ginseng and St. Johns Wort should be avoided as should cooking in aluminum pans.

Conclusion

PD is not curable but is manageable through diet and medications. Education of the patient and caregivers is of paramount importance in working with the prescribed diet and medications. Often these patients get discouraged but it is important for them to realize that they have some control over this disease and can use supportive measures to reduce the side-effects so commonly associated with this neurological disorder. References ​ 1. Agim ZS, Cannon JR. Dietary factors in the etiology of Parkinson’s Disease. Biomed Research International. 2015; http://dx.doi.org/10.1155/2015/672838. 2. Perez-Pardo P, Kliest T, Dodiya HB, et al. The gut-brain axis in Parkinson’s disease: possibilities for food-based therapies. European Journal of Pharmacology. 2017; 817:86-87. http.//dx.doi.org/10.1016/j.ejphar.2017.05.042. 3. Seidl S E, Santiago JA, Bilyk H, Potashkin J.A. The emerging role of nutrition in Parkinson’s disease. Frontiers in aging neuroscience. 2014; 6(36):1-14. Doi.10.3389/fnagi.2014.00036. 4. Pardo P, deJong E, Broersen L M, et al. Promising neurorestorative and gastrointestinal dysfunction after symptom development in the mouse model. Frontiers in Aging Neuroscience. 2017;9(57): 1-12.doi:10.3389/fnagi.2017. 00057. 5. Mischley LK, Lau RC, Bennett RD. Role of diet and nutritional supplements in Parkinson’s disease progression. Oxidative Medicine and Cellular Longevity. 2017. https://doi.org/10.115512017/6405278. 6. Pizzorno JE, Murray MT, Joiner-Bey H, eds. Parkinson’s Disease. In: The Clinician’s Handbook of natural Medicine. 3rd ed St. Louis, Missouri: Elsevier Press; 2016:749-765. 7. Pinto NB, Alexandre B, Neves KR, et al. Neuroprotective properties from Camellia sinensis (Green Tea) and is main bioactive components, epicatechin and epigallocatechin gallate, in the 6-OHDA model of Parkinson’s disease. Evidence based complementary and Alternative Medicine 2015. http://dx.doiorg/10.1155/2015/161092. 8. Mack, JM, Schamne MG, Samoaio Tb, et al. Melatoninergic system in Parkinson’s disease from neuroprotection. Oxidative Medicine and Cellular Longevity. 2016:1-31. 9. Paul R, Phukan BC, Thenmozhi AJ, et al. Melatonin protects against behavioral deficits, dopamine loss and oxidative stress in homocysteine model of Parkinson’s disease. Life Sciences. 2018; 192:238-245. https://doi.org/10.1016/jlfs.2017.11.016.